HALL TICKET NO. 18100006001
LONG CASE:
A 47 year male patient resident of Nalgonda came with chief complaints of abdominal distension and swelling of bilateral lower limbs since 6 months which is gradually increasing since 10 days and fluid discharge from the umbilical area since 2 days and fever since 2 days.
History of present illness
Patient was apparently asymptomatic 18 months back then he noticed abdominal distension which is insidious in onset and gradually progessive in nature and subsequently noticed bilateral swelling of lower limbs , he was hospitalized for one week and took medication which increased his urine output and abdominal paracentesis was done and felt better ,, However he discontinued medicine 6 months back and presented with similar complaints where he was hospitalized and treated conservatively , he was hospitalized 3 months back again with similar complaints , again abdominal paracentesis of 1.5 to 2 lit was done. He is on medication,
the past 10 days he noticed abdominal distension associated associated with swelling of bilateral lower limbs which started at ankle and progressed upto knee,
C/0 of swelling over umbilical region since 3 months insidious in onset, progressive in nature initially of pea nut size now progressed to size of 3* 4 cm where he stratched it and clear yellow fluid started oozing from last 2 days it and it is not associated with blood.
H/0 of fever high grade, intermittent in nature not associated with chills, since 2 days,
H/0 of anorexia, fatigue and generalized weakness since 3 months,,
H/0 of itching present since 3 months, which generalized in onset more on the trunk,,
H/0 of disturbed sleep since one month, where he complained of excessive day time sleepiness and night disturbed sleep,
H/0 of yellowish discoloration of eyes 3 months back now it subsided,
No h/0 of nausea and vomitings,
No h/0 of pain abdomen
No h/0 of decreased urine output
No h/0 of high coloured urine and clay coloured stools.
No history of shortness of breath
No history of blood transfusions
Past medical illness-
History of abdominal distension, swelling of bilateral pedal oedema, and hematemesis one episode 50 ml 18 months back, where he admitted in an hospital for 10 days which relieved with diuretics, abdominal paracentesis and gastric oesophageal ligation was done.
Appendicectomy 25 years ago
No history of hypertension, diabetes, thyroid, epilepsy or seizure disorder.
Personal history-
Diet - mixed
Sleep - disturbed, excessive day time sleep, night time disturbed sleep since one month.
Appetite- decreased.
Bladder habits- regular and normal.
Habits- chronic consumption of alcohol since 20 years daily, country liquor of 500 ml nearly 110gm per day, and whisky of 150 ml per day nearly 50gm per day,
Last binge of alcohol - 3 days before admission he took 100gm.
Summary - Decompensated chronic liver disease secondary to ethanol consumption, with ascites, portal hypertension, hepatic encephalopathy stage 1 and spontaneous bacterial peritonitis.
General examination -
Moderately built and nourished.
Patient is oriented to time, place and person.
GCS - E4 V5 M6
VITALS -
Pulse - 82 beats per minute, regular normal volume, and character, no radio radial or radio femoral delay.
Blood pressure - 100/70 mm Hg, right arm supine position.
Respiratory rate - 18 cpm, thoracoabdominal.
Spo2- 98 % on room air
Jvp - not elevated.
Physical examination-
Pallor - present
Icterus - absent
No cyanosis
No clubbing
No generalized lymphadenopathy
Pedal edema +
Head to toe examination-
Axillary and public hair - sparse.
B/ l parotid enlargement - negative
No fetor hepaticus
No asterixis
No gynaecomastia
Spider nevi - absent
No planar erythema
No leuconchyia
No evidence of xanthoma and xanthelasma.
Flapping tremors - seen.
Inspection -
Oral cavity - No dental caries and no Tobacco staining
Abdomen - flanks full, distension.
Umbilical hernia present
Appendicectomy scar present.
Distened veins present.
No visible peristalsis or no visible pulsations.
Palpation -
Done in supine position with Both Limbs flexed and hands by side of body.
No tenderness or local rise of temperature.
Abdomen - soft.
No gaurding and rigidity
Lower border of liver not palpable.
Spleen not palpable
Kidneys bimanually palpable, ballotable.
Fluid thrill - present
Abdominal girth - 98 cms .
Xiphisternum to umbilicus - 16 cms
Public symphysis to umbilicus - 13cms
Percussion -
Liver span - upper border of liver dullness in 5 th intercoastal space in mid clavicular line, lower border could not be appreciated.
Auscultation:
Normal bowel sounds heard.
No hepatic bruit, venous hum or friction rub.
Examination of external genitilia - No testicular atrophy.
Examination of spine - Normal.
Provisional diagnosis -
Decompensated chronic liver disease
Etiology - chronic ethanol related.
Ascites, SBP, Hepatic encephalopathy
? Hepatorenal syndrome. Esophageal gastric ligation bands were.
CTP SCORE - C
MELD SCORE - 28.
Investigations-
CBP -
HB - 10.7
TLC - 19100,
PLT - 1.50 LAKH
N - 90
CUE -
Albumin- 2+
Sugar- nil
Rbcs- nil
Pus cells - 4-5
RFT -
Blood urea - 116 mg/ dl
Serum creatinine - 4.8 mg/dl
Sodium - 128 meq/l
Potassium - 5.5meq/l
Chloride - 102 meq/l
Uric acid - 5.0
Calcium - 9.1
Phosphorus - 8.0
LFT -
Total bilirubin - 1.63 mg/ dl
Direct bilirubin - 0.40mg/dl
SGOT - 34 IU/L
SGPT - 20 IU/L
ALP - 186 IU/L
Total protein - 5.4 gm/dl
Albumin - 2.06 gm/ dl
RBS- 70mg/dl
Ascitic fluid analysis -
SAAG - 1.74. Serumalbumin - 2.01
Ascitic albumin - 0.36
Ascitic LDH - 120 IU/ L
Ascitic sugar - 52 mg/ dl
Ascitic protein - 0.8 g/dl
Appearance - Clear
Neutrophil count - 405.
Total count - 675
RBCS - Present.
PT - 16 Sec.
APTT - 32sec.
INR - 1.11
Hiv - negative.
Hbsag -negative.
Hcv - negative.
ECG -
X ray -
Treatment given -
1. Tab PAN 40 MG OD
2. TAB. RIFAGUT 550 mg po BD
3. SYP.HEPAMERZ 10 ml Bd
4. SYP. Lactulose 10 ml H/ S
5. Tab Udiliv 300 mg po BD.
6. Inj . Ciprofloxacin 500mg iv Bd
7. Daily abdominal girth.
8. Salt restricted diet.
1. Role of Rifaximine in treating and preventing hepatic encephalopathy.
https://www.nejm.org/medical-articles/original-article.
SHORT CASE - 1:
A 45 year old female patient farmer by occupation
Resident of Nalgonda came to casuality with complaints of vomitings and abdominal pain since 4 days
HISTORY OF PRESENTING ILLNESS
Patient was apparently asymptomatic 6 days back then she was allegedly bitten by snake on her right lateral foot at 7.30 pm while she was cooking, she was taken to local hospital and started on treatment (20 min whole blood clotting test was positive started her on Anti snake venom later shifted here,
C/0 of abdominal pain since 5 days, periumbilical in location, non radiating pain aggravated with food intake relieved with medications.
C/0 of vomitings since 5 days. 3 to 4 episodes per day, containing non digested food particles non bilious, non projectile in nature,
C/0 swelling of right foot non pitting type insidious in onset progressed upto ankle and releived in 2 days
C/0 of anorexia, myalgias, fatigue and generalized weakness from 5 days,
No C/0 of pain at site of bite.
No H/0 of blood oozing from site of bite, epistaxis, hematemesis, Malena.
No H/0 of decreased urine output or cola coloured urine.
No h/o of shortness of breath, chest pain, palpitations,
No H/o of loose stools, constipation
No h/0 of weakness of limbs , drooling of saliva, ptosis
No h/0 of SOB, PND or orthopnea.
Past history -
No histoy of hypertension, diabetes, thyroid, epilepsy, tuberculosis and asthma.
Personal history-
Diet - mixed
Sleep- adequate
Appetite - normal
Bowel and bladder -
Not a alcoholic or smoker
Summary -
45 year old female patient alleged to snake bite, presententing with Nonoliguric Acute kidney injury.
General physical examination-
Patient was conscious, coherent, well oriented to time place and person
Pallor - present
No Icterus
No clubbing, no cyanosis
No lymphadenopathy
No edema.
Vitals -
Temp - 98.6 F (measured in axilla).
PR- 82 beats per min, normal in rhythum, character and volume ,no vessel wall thickening , no radio radial or radio femoral delay.
Bp - 140/ 90 mm hg, measured in right upper arm in supine position.
RR- 16 cpm.
Cvs - S1, S2 heard, no jvp rise, no murmurs heard, apical impulse-
Rs - Non vesicular breath sounds heard, equal bilateral air entry , no added sounds.
P/ A - soft, no tenderness elicited,
No mass felt, No organomegaly. Bowel sounds heard.
CNS - Higher mental functions are normal.
Tone - norma
power - 5/5 in both limbs,
All superficial and deep reflexes are normal
Sensory and cerebellar system - intact 
INVESTIGATIONS-
COMPLETE BLOOD PICTURE-
HB - 8.5 gm/dl.
Platelet count- 63000
WBC count - 9000
RBS- 113mg/dl.
Serum creatinine - 7.4 mg/dl.
Blood urea - 166mg/dl.
BUN - 77.5
Sodium - 124meq/l
Potassium - 3.9meq/l
Chloride - 75meq/l
Spot urine protein creatine ratio - 0.13.
Spot urine sodium - 229 mmol/ L .
Complete urine examination-
Colour - pale yellow
Pus cells - 2-3
Rbcs - nil
Albumin - nil
Bleeding time - 2min 15 secs
Clotting time - 4 min 45 secs.
Total bilirubin - 1.0 mg/ dl
Albumin - 4.5 gm
SGPT - 34 ( 15- 40)
SGOT - 24
ALP - 90 IU/L
ABG -
PH - 7.403
Hco3- 16.7
Pco2-. 22.1
Spo2- 97.2 %
Urine protein creatine ratio,- 0.13
Urinary sodium - 229.
X ray -
ECG -
USG -
KIDNEY SIZE - Normal, increased echotexture and mild perinephric fluid likely inflammation.
Provisional diagnosis -
Acute kidney injury, secondary to acute tubular necrosis, due to snake bite.
Treatment -
1. 4 sessions of
haemodialysis
2. Inj zofer 4 mg TID
3. Inj pan 40 mg Od
4. Strict input / output
charting.
High dose vs low dose anti snake venom
http://www.ncbi.nlm.nih.gov/pubmed/1563371
SHORT CASE - 2:
A 57 year oldfemale patient came with complaints of weakness of both lower limbs Since 3 months. Reduced sensations in both lower limbs since 3 month.
Patient was apparently asymptomatic 3 months back when she was doing her routine daily work, she developed weakness of left limb in the form she had difficulty in raising the left leg, she also had difficulty in climbing up and down stairs, difficulty in getting up from squatting position.
But she was able to walk with difficulty
5 days later she noticed difficulty in gripping chappals and to walk with chappals in both lower limbs .
10 days later she Noticed similar weakness in right leg also .
Both her upper limbs were normal, She was able to lift her head from pillow,
7 days later she developed numbness and burning sensations below the nipple area, and both lower limbs.
She had difficulty in feeling her clothes and had difficulty in differentiating hot and cold water below the nipple area.
No H/0 of improvement of weakness as the day progress .
H/0 of low backache insidious in onset dull aching pain diffusely felt around lumbosacral area, gradually progessive in nature, non radiating since last one month, pain worsening with movement and receiving pain killers,,
Walking difficulty was not increasing in dark.
No H/0 of involuntary movements
No H/0 of altered sensorium, No H/0 of disorientation.
No H/0 of double vision
No H/0 of reduced sensations over face and she was able to chew food.
She was able to perceive the smell normally.
She was able to Close the eyes and no history of deviation of angle of mouth or drooling of saliva.
she was able to hear properly, no vertigo.
No H/0 of dysphagia, nasal regurgitation.
No H/0 of dysarthria.
She was able to feel the bladder sensation, initiate micturition and evaquate bladder completely, no history of post voidal urine sensation or post voidal dribbling.
No H /0 of bowel incontinence or constipation.
No H/0 of altered sweating pattern.
No H/0 of fever, headache, seizures, weight loss, skin rashes, and recent vaccination.
She was admitted in local hospital and got treatment but no improvement.
Past history:
she had a h/o thyroid surgery 4 years back.
No h/o hypertension, diabetes mellitus, CAD, Asthma
Personal history:
diet is mixed
Appetite is regular
Bowel and bladder are regular
Sleep adequate
No addictions
No significant family history.
Summary:
A 57 year old Female patient with no comorbities and no trauma history presented with subacute to chronic paraplegia started asymmetrically associated with no cranial nerve or autonomic involvement.
GENERAL EXAMINATION:
Patient is c/c/c and oriented.
Thin built and moderately nourished
Temperature: Afebrile
Pallor-absent
Icterus-absent
No cyanosis, clubbing and lymphadenopathy
Bp:90/60mmhg
PR:75 bpm regular in rhythum and character, no radio femoral delay.
CVS: S1 and S2 heard, no murmurs
RS: BAE present NVBS.
P/A: Soft and Nontender, bowel sounds heard.
CNS EXAMINATION:
Speech is normal
Cranial nerves examination: Normal
Motor examination
TONE
UL N. N
LL. Decreased Decreased.
POWER
UL. 5/5. 5/5
LL. 1/5 1/5
REFLEXES
Superficial reflexes
Corneal Present. Present
Conjuctival Present. Present
Abdominal upper absent
Lower absent
Beevors sign - negative.
Deep tendon reflexes
Biceps present present
Triceps present present
Supinator. Present present
Knee. Exaggerated diminished
Ankle. Exaggerated diminished
Plantar. Extensor extensor.
Sensory system examination-
pain, temp, vibration, joint position, and fine touch - bilaterally reduced below the level of nipples.
Cerebellar signs are normal.
Gait could not be assessed.
No neck rigidity
No signs of meningeal irritation
Spine - tenderness felt at T6- L3 spine.
No Gibbus
No Kyphosis or scolios.
Provisional diagnosis-
Extra medullary compressive myelopathy
Cadua equina syndrome.
Motor level - T6
Sensory level- T6
REFLEX LEVEL - T6.
Propable etiology - Metastasis.
Investigations
CBP -
HB - 12.0
TLC - 6000
PLT - 2.4 lakhs
CUE -
Albumin- trace
Sugar- nil
Rbcs- nil
Pus cells - 4-5
RBS- 116 mg/ dl
RFT -
Blood urea - 28 mg/ dl
Serum creatinine - 0.8 mg/dl
Sodium - 136 meq/l
Potassium - 3.9meq/l
ECG -
MRI SPINE:
August 09, 2021
THESIS
TITLE:
ASSESSMENT OF SERUM MAGNESIUM AND ITS OUTCOME IN ACUTE ISCHEMIC CEREBROVASCULAR ACCIDENTS.
INTRODUCTION:
Magnesium depletion in the diet is more prevalent than generally expected. In
industrialised and developing countries it remains to be most common nutritional
problems. This may be due to result of current changes in agricultural practices, food
preparation techniques and dietary changes. WHO and other health agencies states that
more than 75 to 80% of people do not consume the recommended daily intake of
magnesium (1)
Magnesium depletion is considered to be most under diagnose electrolyte
abnormality in current medicine. The prevalence of magnesium deficiency in hospital
settings has been found to be 7 to 11 %. 40% of patients deficiency also coexist with other
electrolyte abnormalities. (2)
Magnesium deficiency is more common in alcoholics, young people and people who
receive certain medications. It is associated with hypertension, diabetes, coronary heart
disease, stroke, osteoporosis due to thrombogenic and atherogenic disruption of arterial
and cardiac integrity. (3)
The National institute of Health website publishes, in human body for the correct
metabolic function more than 350 enzymes magnesium is needed. “Magnesium helps in
proper functioning of muscles and nerves maintains a strong immunity against infections,
supports bone integrity and keeps the heart work in regular rhythm It regulates blood sugar
values , keeps the blood pressure in control, has a role in protein synthesis and energy
metabolism. Interest is gaining in role of magnesium in the prevention and treatment
of diabetes, hypertension, cardiac, cerebral disorders”. Thus deficiency is considered to
be epidemic deficiency.(4)
In acute cerebrovascular accidents, there occurs a rapid loss of brain magnesium and
potassium levels with rapid uptake of sodium and calcium channels, the lower the
magnesium and potassium concentrations the greater the magnitude of cerebral arterial
contraction.
Interruption of cerebral blood flow will lead on to ischemic cell death causing ATP
depletion and ischemic depolarisation leading to excessive calcium entry which causes
vasospasm.
Cerebral blood flow interruption causes release of excitatory glutamate through NMDA
receptors, which causes influx of calcium and sodium leading onto production of free
radicals and initiation of inflammatory response.
Magnesium exerts neuroprotection in the following ways:
1. It‟s a natures physiologic calcium blocker antagonises calcium mediated metabolic
process.
2. It decreases the release of excitatory neurotransmitter
3. It increases the release of inbitory neurotransmitter
4. It relaxes vascular smooth muscle
5. It decreases platelet aggregation.
AIMS AND OBJECTIVES OF THE STUDY:
AIM OF THE STUDY:
To Study serum Magnesium and outcome of patients In Acute ischemic cerebrovascular
accidents.
OBJECTIVES OF STUDY:
1. To detect the serum magnesium levels in patients of Acute ischemic cerebrovascular
Accidents.
2. To detect the outcome ofacute ischemic stroke patients in accordancewith the
magnesium levels.
VARIABLES MEASURED IN STUDY:
MODIFIED RANKIN SCALE:
The Rankin scale is named after the Scottish physician JohnRankin who made this
scale in view to access the disability of thepatient with specific reference to morbidity
of the patient. The scalewas made to access the patient who suffered from stroke to access
the global disability of these patients was later to be used in clinicaltrail and the name
Modified Rankin scale (mRs).
The Modified Rankin scale was used initially in a study in Great Britain for patients suffering
from TIA. After this the scale has gained popularity and now it is widely used to access the
functional outcomes of patients who suffer from stroke.
Advantages of MRS scale:
1.Easy to perform
2. Takes about five minutes to perform
3. It has close correlation with other stroke scale like the NIHSS scale and theBI
4. The volume of infarct correlates well with the imaging findings of patients with
CVA
5. It has six point score which correlates well with the outcome of patients
6. As in the case of NIHSS there are various mobile phone apps, DVDs, online
certificate courses for Learning the scale
Limitations of the MRS scale:
1. As there are only six point score it is less probable to change than other stroke
scales
2. The specificity of the scale is less
3. Inter observer variability is high with respect to this scale
4. Detailed training in scripted interviews is required to improve the reliability and the
consistency of the scale
PATIENTS AND METHODS:
Methods and study design:
This was a observationl study, done in patients admitted in medical wards of Kamineni
institute of medical sciences, Narketpally, Nalgonda, conducted from October 2018 to September 2020. The study will be approved by the ethical Committee of Kamineni
Institute of medical sciences, Narketpally.
INCLUSION CRITERIA:
1. Diagnosis of ischemic stroke based on history , physical. examination and initial
CT/ MRI of Brain or delayed
CT /MRI scan of brain where first scans were normal.
2. Age greater than 40 years
3. Cerebrovascular accidents occurring less than 72 hours.
EXCLUSION CRITERIA:
4. Chronic kidney disease
5. Alcoholic liver disease
6. Thyroid disorders – hypo/hyperthyroidism
7. Chronic diarrhea
8. Patients on drugs that affect serum magnesium levels like diuretics, digoxin and
drugs like amphotericin B
aminoglycosides
9. Age less than 40 years.
DATA COLLECTION AND METHODS:
patients who have got admitted in medicine ward, in the Institute of Kamineni institute of medical sciences, Narketpally, Nalgonda in Department of General medicine, an observational study was conducted on acute cerebrovascular accident patients for a period of two years. Patients selected for clinical study as per inclusion and exclusion criteria. Informed consent was obtained from the relatives of the cases. Detailed history taking and clinical examination was done. Around 2ml of venous blood was collected from the patients. Blood was allowed to clot and serum was separated by centrifugation. Serum levels of Magnesium were estimated using calorimetric method. Neurological status of the patients suffering from cerebrovascular accidents was assessed at the time of admission and at the time of discharge was assessed using modified Rankin Scale(mRS) and Glasgow coma scale.
STATISTICAL METHODS:
Present study results were obtained by using SPSS statistics 20.0 software, following statistical methods are used in this study:
1. MEAN: It is simplest measure of central tendency and is the arithmetic average of observations.
For a ungrounded data, mean is calculated by
MEAN: Sum of all observations
Number of observations
X = ∑X
n
For grouped data, mean is calculated by
X = ∑ fx
n
Where f is the frequency
x is mid point of class interval
n is total number of observations
2. STANDARD DEVIATION: It is a measure of the magnitude of the variation
present in set of data. It is known as root mean square deviation because it is square
root of the mean of squared deviations from arithmetic mean. It is a summary
measure of the differences of each observation from mean of all the observations.
S = d2
(n-1)
3. Level of significance: The magnitude of risk of making a wrong conclusion of rejecting the null hypothesis that the two groups are from same population is fixed in terms of probability level „p‟ and is known as level of significance.
LINK TO COMPLETE THESIS WITH MASTER CHART:
MASTER CHART
August 09, 2021
ACADEMIC PRESENTATIONS
S.NO | DATE | TOPIC | PRESENTER WITH LINK |
1. | 16/06/2020 | A case of emphysematous pyelonephritis | |
2. | 8/ 7/2020 | A case of multiple liver abscess | |
3. | 28/01/2021 | Discussion on hyponatremia | |
4. | 11/07/2020 | Thesis discussion of assessment of serum magnesium and its outcome in acute ischemic cerebrovascular accidents | |
5 | 28/07/2019 | Fluorosis central meet seminar | |
6. | 29/01/2021 | Polyarthritis | |
7. | 19/12/2019 | CKD on MHD. MORTALITY MEET | |
8. | 12/03/2019 | Acute pancreatitis walled of necrosis Morbidity meet | |
9. | 17/12/2019 | Cardiogenic shock – pulmonary edema and pulmonary embolism – Mortality Meet | |
10. | 13/02/2019 | Role of amlodipine in controlling hypertension of stroke patients . Journal club |
CASE PRESENTATION
VIDEO LINKS
HALL TICKET NO: 18100006002
CASE PRESENTATIONS
LONG CASE;
A 70 years old female patient residing in Nalgonda, is a homemaker, presented to OPD with complaints of- loss of appetite since one week,
- generalised weakness since one week
- fever since 5 days
-burning micturition since 5days
History of present illness-
Patient was apparently asymptomatic one week back then she gradually developed loss of appetite since one week which was not associated with nausea, vomiting, associated with generalised weakness fever since 5 days which was high grade associated with chills and rigors, no diurnal variation, relived on taking medication, not associated with headache, cold, cough. She also started experiencing burning micturition since 5 days associated with low backache, no history of dark coloured urine or blood in urine
no h/o cold, cough, chest pain, palpitations, shortness of breath, pedal edema, reduction in urine output, diarrhoea, constipation, vomiting, nausea, pain abdomen
Past history:
she has been having similar episodes since 2016
she had 1st episode in 2016 it started with fever which was high grade associated with chills and rigors, associated with loss of appetite which were followed by loss of consciousness. she was immediately rushed to a local hospital where the attenders were told that she had high blood pressure and had high blood sugars. she was diagnosed with UTI and was treated with parenteral antibiotics for 5 days and was discharged on oral antibiotics which she took for one week. since then she had been having recurrent episodes of UTI 2-3times every year. after the 2nd or 3rd episode she started having urinary incontinence for which she consulted a urologist and was said to have weakness of pelvic floor muscles and was advised pelvic floor muscle strengthening exercises.
28 years back she underwent hystrectomy
25 years back she had complaints of generalised weakness
↓
went to a diagnostic center and got few investigations done
↓
consulted a physician and was diagnosed with type 2 diabetes mellitus and was started on OHAs
she did not take OHAs regularly
During that time she was residing in Saudi Arabia and her husband took her to regular check ups almost every weekend during that period he sugars were under control with OHAs
↓
In 2007 they moved back to India in 2010 she had uncontrolled blood sugars for which she was started on insulin, she started using insulin pen
↓
In 2013 she consulted an endocrinologist and was started on injections Humalog (insulin Lispro) 28 units in the morning and Basalog (insulin Glargine) 20 units at night
↓
started having tremors, weakness, excessive sweating, and excessive hunger (had recurrent hypoglycemic attacks) during which he son Dental surgeon advised her to reduce the dose of Insulin lispro to 20 units
↓
reviewed with the same endocrinologist and was advised to stop Insulin glargine and was told to take insulin lispro in the evening also
↓
had recurrent episodes of UTI and got hospitalised for the same
↓
10 years back she had chest pain for which she was taken to a cardiologist and was diagnosed with angina and was started on antiplatelets, statins and isisorbide dinitrate (SOS), tab febuxostat 40mg (for joint pains), vitamin D3 supplementation, and was also advised tab nitrofurantoin for 20 days since then she was on a regular follow up with the cardiologist every 3 months
She also started having complaints of tingling and numbness in her lower lower limbs and was diagnosed with peripheral neuropathy secondary to diabetes mellitus and was startedon tab. neuroprime plus (alpha lipoic acid, thiamine, mecobalamin, elemental chromium)
was also diagnosed with CKD and anemia
↓
Diagnosed with Hypothyroidism 5 years back and was started on tab. levothyroxine 50 mcg daily before breakfast
↓
blood sugars were not under control in 2020 consulted an endocrinologist was started on sitagliptin 50mg and metformin 1000mg everyday morning before break
↓
in 2020 she was treated at home by her son for the similar episodes
↓
in 2021 march she had complaints of fever, cough and was diagnosed with COVID 19 infection and was hospitalized
there she was treated with Injection remdesivir for 5 days along with parenteral steroids and was later discharged on oral prednisolone and was gradually tapered over 10 days and then stopped
↓
In July she again had another episode of UTI and was again hospitalized
↓
was brought to our center
Personal history: married with 8 children - 4 sons and 4 daughters all are well at present,
no addictions - non smoker non alcoholic
sedentary habit
adequate sleep
no bowel abnormalities
family history- not significant
treatment history:
used insulin lispro (50%) + insulin lispro protamine 25 units in the morning and evening subcutaneously
used - Tab Ecospirin AV 75/10 mg H/S
tab Met -XL initially 25 mg for few years then 5o mg once daily
tab. feburic acid 40mg
tab tenegliptin 20mg then changed to tab sitaglipten 50mg + metformin 1000mg once daily
vitamin D3supplementation
used multiple antibiotics for recurrent UTI- nitrofurantoin, clarithromycin, piptaz, meropenem, levofloxacin
tab isosorbide dinitrate SOS
PROVISIONAL DIAGNOSIS:
A 70 years old lady with Recurrent complicated UTIs with peripheral neuropathy, secondary to diabetes mellitus (type 2) with hypertension with hypothyroidism known case of ischaemic heart disease.
GENERAL EXAMINATION:
patient is conscious, coherent, cooperative and oriented to time, place and person
patient is lying comfortably in supine position
patient is obese and well nourished
Height- 151 cms
Weight - 57 kgs
BMI - 25.0 kg/m2
face- wrinkled
eye- no abnormalities, baggy lower eyelids, pallor present, no xanthelasma or xanthomas
no cyanosis
oral cavity- lost all teeth, mucosa appears normal
nails- normal, no clubbing
no thyroid enlargement
no lymphadenopathy
neck veins- not distended
skin- normal, No pigmentation, No scars, No atrophic changes
pulse- 110 beats per minute in supine position in right radial artery, regular rhythm, high volume, vessel is thickened, all other peripheral pulses are felt and are normal
BP: 110/80 mmHg in Right arm in supine position
100/80 mmHg in standing position
Respiration-- 20 breaths per min, thoraco-abdominal type
temperature- normal at the time of examination
feet-no pedal edema, no ulcers or calluses
GENITOURINARY SYSTEM EXAMINATION:
per abdomen- no abnormalities, no visible scars and sinuses
foleys catheter is insitu and is connected to urobag
no renal lump felt
renal angle- no tenderness
urinary bladder- empty
local examination - pubic hair-sparse distribution
labia majora, minora- atrophied
external uretheral meatus- no discharge, healthy
per vaginal examination bimanual examination
bilateral fornices free, non tender
anterior fossa normal
posterior fossa normal
Vault intact - no palpable masses felt, no tenderness
NERVOUS SYSTEM EXAMINATION
patient is conscious, cooperative, alert and oriented to time place and person
cranium and spine -normal, no abnormalities
speech- normal
Recent and remote memory intact
1. CRANIAL NERVES
CRANIAL NERVE | TEST | RIGHT | LEFT |
I | Sense of smell i) Coffee ii) Asafoetida |
+ + |
+ + |
II | i) Visual acuity – Snellens Chart ii) Field of vision – Confrontation test iii) Colour vision – Ishihara chart iv) Fundus | 6/6 Normal Normal Normal | 6/6 Normal Normal Normal |
III, IV, VI | i) Extra-ocular movements ii) Pupil – Size iii) Direct Light Reflex iv) Consensual Light Reflex v) Accommodation Reflex vi) Ptosis vii) Nystagmus viii) Horners syndrome | full 4mm Present Present Present Absent Absent No | full 4mm Present Present Present Absent Absent No |
V | i) Sensory -over face and buccal mucosa ii) Motor – masseter, temporalis, pterygoids iii) Reflex a. Corneal Reflex b. Conjunctival Reflex c. Jaw jerk | Normal Normal
Present Present Present | Normal Normal
Present Present Present |
VII | i) Motor – nasolabial fold hyeracusis occipitofrontalis orbicularis oculi orbicularis oris buccinator platysma ii) Sensory – Taste of anterior 2/3rds of tongue(salt/sweet) Sensation over tragus iii) Reflex – Corneal Conjunctival iv) Secretomotor – Moistness of the eyes/tongue and buccal mucosa |
Present Absent Good Good Good Good Good
Normal
Normal
Present Present
Normal |
Present Absent Good Good Good Good Good
Normal
Normal
Present Present
Normal |
VIII | i) Rinnes Test ii) Webers Test
iii) Nystagmus | Positive Not lateralised
Absent | Positive
Absent |
IX, X | i) Uvula, Palatal arches, and movements
ii) Gag reflex iii) Palatal reflex | Centrally placed and symmetrical
Present present |
|
X1 | i) trapezius ii) sternocleidomastoid | Good Good | Good Good |
XII | i) Tone ii) Wasting iii) Fibrillation iv) Tongue Protrusion to the midline and either side | Normal No No Normal | Normal No No Normal |
MOTOR SYSTEM:
Right. Left
Bulk: inspection UL normal normal
LL normal normal
palpation. UL Normal normal
LL normal normal
Tone: UL normal. Normal
LL. normal. normal
Power UL. 5/5. 5/5
LL: 5/5 5/5
Reflexes.
Superficial reflexes
Right. Left
Corneal. P P
Conjunctival P. P
Abdominal. + +
Plantar flexor flexor
Deep tendon reflexes
Right. Left
Biceps jerk. + +
Triceps jerk . + +
Supinator jerk. + +
Knee jerk + lost
Ankle jerk lost lost
SENSORY SYSTEM
RIGHT. LEFT
SPINOTHALAMIC
crude touch. UL lost in distal parts on both sides
LL lost in distal parts on both sides
pain. UL- lost in distal parts on both sides
LL- lost in distal parts on both sides
temperature. lost in distal parts on both sides in both limbs
post:
fine touch. lost in distal parts on both sides in both limbs
vibration. lost in distal parts on both sides in both limbs
position sensor. lost in distal parts on both sides in both limbs
cortical
2 point discrimination and tactile localization- could not be assessed
CEREBELLUM
titubation - absent
ataxia - absent
coordination- normal
no nystagmus
Romberg's sign could not be checked as patient was feeling weak
NO SIGNS OF MENINGEAL IRRITATION
AUTONOMIC FUNCTIONS:
positional tachycardia- absent
no orthostatic hypotension
sweating- normal
gait: could not be assessed as she was feeling weak
Investigations
FINAL DIAGNOSIS:
1. Recurrent complicated urinary tract infections
2. Complicated Fungal UTI
3. Asymmetric Peripheral neuropathy secondary to Diabetes mellitus type 2
4. Diabetic nephropathy
5. known case of Ischaemic heart disease, Hypertension, Hypothyroidism
SHORT CASE- 1:
A 43 old male patient resident of Nalgonda, farmer by occupation, presented to casualty with complaints of:
Low grade Fever since 1 year.
Cough with sputum since 1 year
Complaints of neck pain since 6 months
Weakness of all both lower limbs since 6 months.
HOPI:
Patient was married at age of 25 and have 3 children, one son and two daughters. He is farmer by occupation. He is occasional alcoholic and chronic smoker (1-2 packs/day) since 20 years. He was apparently alright till 33 years of age, then in view of generalised weakness pt went for routine evaluation and got diagnosed with diabetes mellites- type 2 and is using OHA since 10 years. He takes his medication regularly.
Patient had history of fever since 1 year which was low grade not associated with chills and rigors, intermittent, associated with diurnal variation and night sweats.
He also complains of cough with scanty white color, mucoid expectorant since 1 year, non foul smelling, non blood tinged. No diurnal variation of cough and no chest pain.
He went to local rmp and got symptomatic treatment.
He later developed neck pain, which was sudden in onset gradually progressive. No history of trauma. No radiation.
He then developed weakness of both lower limbs which was insidious in onset, gradually progressive in nature over 6 months. He had difficulty in standing and walking. No history of upper limb weakness.
H/o difficulty in standing from sitting position present.
H/o difficulty in climbing stairs present.
H/o slippage of chappal while walking without knowledge
H/o difficulty in sqatting present .
No h/o difficulty in getting up from lying down.
no h/o difficulty in holding pen/buttoning/unbuttoning
no h/o difficulty in breathing
no h/o difficulty in lifting the head off the pillow
no h/o difficulty to roll over the bed
no h/o involuntary movements.
no h/o fasciculations/muscle twitchings .
h/o sensory deficit in feeling clothes present.
H/o loss of hot/cold sensations present.
H/o tingling and numbness in UL & LL present.
H/O band like sensation present.
H/o cotton wool sensations present.
no h/o low backache
no h/o trauma
no h/o giddiness while washing face
no h/o urgency/hesitancy/increased frequency of urine
no h/o urinary incontinence
h/o fever/
No h/o nausea/ vomiting/diarrhea
no h/o seizures
no h/o spine disturbances
no h/o head trauma
no h/o loss of memory
no h/o abnormality in perception of smell
no h/o blurring of vision
no h/o double vision/difficulty in eye movements
no h/o abnormal sensation of face
no h/o difficulty in chewing food
no h/o difficulty in closing eyes
no h/o drooling of saliva
no h/o giddiness/swaying
no h/o difficulty in swallowing
no h/o dysphagia/dysphasia
no h/o tongue deviation
no h/o difficulty in reaching objects
no h/o tremors/tongue fasciculations
no h/o incoordination or difficulty in performing task
no h/o fever/neck stiffness
no h/o loss of consciousness and involuntary movements, no h/o irrelevant talk, no slurring of speech, no h/o memory loss and hallucinations .no sleep disturbances.
Past history:
No h/o similar complaints in past.
K/C/O DM-2 since 10 years on Glimi -m1 tablet.
Not a known case of HTN/EPILEPSY/CVA/CAD/TB
FAMILY HISTORY - NOT SIGNIFICANT.
SURGICAL HISOTRY - No previous surgeries or blood transfusions.
Personal history:
Mixed diet with normal appetite and normal bowel/bladder movements
H/o alcohol consumption since 90ml weekly twice since 20 years.
H/o smoking (1-2 packs per day) since 20 years.
Summary:
Insidious, progressive bilateral lower limb weakness with paresthesia.
General Examination:
He is a thin built man, who was conscious, coherent
PR of 80bpm, regular rhythm, normovolemic .
Bp - 110/80mmhg
Temp - 98.3 F
SpO2 - 99%
RR - 22 cpm
GRBS - 120 mg/dl.
Head to toe examination:
Hair - Black, thick, non-easily pluckable. No lesions over the scalp.
Eyes - No pallor, no icterus.
General head & neck examination - No abnormalities. No lymphadenopathy.
Axial- Tenderness over cervical spine +
Fingers & Nails - Clubbing +
Lower limbs - No pedal edema.
No neuro -cutaneous markers noted.
CNS EXAMINATION:
HMF-
Patient conscious, co -operative, coherent.
Oriented to place/time/person
no h/o aphasia/dysarthria
no h/o dysphonia
Recent and remote memory intact.
no h/o emotional lability.
1. CRANIAL NERVES
CRANIAL NERVE | TEST | RIGHT | LEFT |
I | Sense of smell i) Coffee ii) Asafoetida |
+ + |
+ + |
II | i) Visual acuity – Snellens Chart ii) Field of vision – Confrontation test iii) Colour vision – Ishihara chart iv) Fundus | 6/6 Normal Normal Normal | 6/6 Normal Normal Normal |
III, IV, VI | i) Extra-ocular movements ii) Pupil – Size iii) Direct Light Reflex iv) Consensual Light Reflex v) Accommodation Reflex vi) Ptosis vii) Nystagmus viii) Horners syndrome | full 4mm Present Present Present Absent Absent No | full 4mm Present Present Present Absent Absent No |
V | i) Sensory -over face and buccal mucosa ii) Motor – masseter, temporalis, pterygoids iii) Reflex a. Corneal Reflex b. Conjunctival Reflex c. Jaw jerk | Normal Normal
Present Present Present | Normal Normal
Present Present Present |
VII | i) Motor – nasolabial fold hyeracusis occipitofrontalis orbicularis oculi orbicularis oris buccinator platysma ii) Sensory – Taste of anterior 2/3rds of tongue(salt/sweet) Sensation over tragus iii) Reflex – Corneal Conjunctival iv) Secretomotor – Moistness of the eyes/tongue and buccal mucosa |
Present Absent Good Good Good Good Good
Normal
Normal
Present Present
Normal |
Present Absent Good Good Good Good Good
Normal
Normal
Present Present
Normal |
VIII | i) Rinnes Test ii) Webers Test
iii) Nystagmus | Positive Not lateralised
Absent | Positive
Absent |
IX, X | i) Uvula, Palatal arches, and movements
ii) Gag reflex iii) Palatal reflex | Centrally placed and symmetrical
Present Present |
Present Present |
X1 | i) trapezius ii) sternocleidomastoid | Good Good | Good Good |
XII | i) Tone ii) Wasting iii) Fibrillation iv) Tongue Protrusion to the midline and either side | Normal No No Normal | Normal No No Normal |
MOTOR SYSTEM :
Right. Left
Bulk: inspection normal. Normal
palpation. Normal. Normal
Measurements U/l 28cm. 28cm
L/L 37cm. 37 cm
Tone: UL hypertonia hypertonia
LL. hypertonia. hypertonia
Power UL. 4/5. 4/5
LL:
iliopsoas 3/5. 3/5
adductor femoris 3/5. 3/5
gluteus medius 3/5. 3/5
gluteus maximus 3/5. 3/5
hamstrings 3/5. 3/5
quadriceps femoris 3/5. 3/5
tibialis anterior. 3/5. 3/5
tibialis posterior. 3/5. 3/5
peroneii. 3/5. 3/5
gastronemius. 3/5. 3/5
extensor -
digitorum longus. 2/5. 2/5
flexor digitorum longus 2/5. 2/5
Reflexes.
Superficial reflexes
Right. Left
Corneal. P P
Conjunctival P. P
Abdominal. + +
Plantar EXTENSOR EXTENSOR
cremasteric. + +
Deep tendon reflexes
Right. Left
Biceps. +3 +3
Triceps. +3 ++3
Supinator. +3 ++3
Knee +3 +3
Ankle. +3 +3
Clonus - both knee and ankle present
SENSORY SYSTEM
RIGHT. LEFT
SPINOTHALAMIC
crude touch. N. N
pain. UL- N N
LL- - -
temperature. - -
post:
fine touch. - -
vibration. - -
position sensor. - -
cortical
2 point discrimination - -
tactile localisation. - -
CEREBELLUM
titubation - absent
ataxia - absent
hypertonia. present present
Rombergs sign-
Respiratory system examination:
Inspection
Rt supraclavicular hollowness
Movements of chest appears to be reduced on right side in supraclavicular region
Palpation vocal fremitus decreased in rt supraclavicular area
Percussion
Dull note in rt supraclavicular and suprascapular region
Auscultation
Wheeze in bilateral lung fields on presentation
Crepitations in left infra axillary area and left infrascapular area.
CARDIO VASCULAR SYSTEM: S1S2 heard.
No murmurs. No palpable heart sounds.
PER ABDOMEN -
SOFT, NO ORGANOMEGALY.
NO GUARDING AND RIGIDITY.
BOWEL SOUNDS PRESENT.
INVESTIGATIONS:
Hemoglobin - 12g/dl
TLC - 10,600 cells/cumm
Platelets - 2.90 Lakhs/cumm
Peripheral smear - Normocytic Normochromic blood picture
ESR - 60mm in 1st hour
HBsAg, HIV, HCV - Negative
RBS - 112 mg/dl
Blood Urea - 43 mg/dl
Serum creatinine - 1 mg/dl
Serum Potassium - 4.1 mg/dl
Serum Sodium - 138 mg/dl
Serum Chloride - 100 mg/dl
Complete Urine Examination - No abnormalities
Sputum for Culture & Sensitivity:
Gram stain, Direct smear: Plenty of inflammatory cells (more than 20/hpf). Few epithelial cells, 1-2/hpf.
Plenty of gram positive cocci in pairs in short chains seen.
Impression- Normal flora grown.
FINAL DIAGNOSIS:
CHRONIC BILATERAL SYMMETRICAL MOTOR SENSORY BOTH PROXIMAL AND DISTAL MUSCLE WEAKNESS SECONDARY TO CERVICAL CORD COMPRESSION AT C4 C5 SECONDARY TO TUBERCULOSIS
K/c/o - DM -2
SHORT CASE- 2:
35 year old man working as a food caterer presented to our OPD with the chief complains of Dyspnea at rest since 5 day
Cough with expectoration since 5 days
Bilateral pedal edema since 4 days
Abdominal distension since 3 days
He was a regular alcoholic since the past 10 years and an occasional smoker. He apparently was completely alright until one morning in November 2019 when he had high fever with chills and visited a local hospital where he got admitted, he says the fever was intermittent and more at nights and was often followed by sweating and was diagnosed with malaria for which he received treatment.
In Dec 2019, the following month, he says he started feeling breathless while climbing up the stairs which progressed over the next 5 days to such an extent that he even felt dyspneic even at rest and had dry cough on and off. He says that his dyspnea and cough aggravated on lying in bed. He gradually developed bilateral pedal edema followed by abdominal distension over the next few days which alarmed him and he decided to pay a visit to a doctor. He visited a local hospital and was put on some medications (no documentation) which patient couldn't recall of. Since it did not improve his symptoms he visited our hospital in January 2020.
He however gave no complaints of palpitations, nausea, vomiting, profuse sweating.
He also gave no complaints of reduced urine output, hematuria, frothy urine.
No complaints of burning micturition, diarrhea, vomiting, pain abdomen.
PAST HISTORY:
Since the past 10 years he has been consuming around 180 ml of whiskey everyday. He also tells that he would occasionally smoke cigarette once in a while along with his friends. In those 10 years he never paid a visit to his hometown due to financial issues and decided not to get married anytime soon as he wanted to settle the financial issues his family was facing.
Not a known case of Diabetes, Hypertension, Also no history of CAD, CVA, Bronchial Asthma, Pulmonary Koch's.
PERSONAL HISTORY:
Patient was born and brought up in ***. He was born to a farmer and a housewife. He has 2 elder siblings, his elder sister is married to an advocate and has 2 children and his elder brother is working as a software engineer. He pursued his degree in electronics but was not successful in finding a job in this branch, so he moved to another state 10 years back and started working in a food catering business along with his friends. During his stay outside his hometown, he says he used to often feel lonely and used to often consume whiskey along with his friends which got to a point that he started consuming around 180 ml of whiskey everyday and would occasionally also smoke cigarettes.
He has been having disturbed sleep because of the financial issues his family has been facing. His appetite has increased and more often consumes outside food.
Since the past 10 years he has been consuming around 180 ml of whiskey everyday. He also tells that he would occasionally smoke cigarette once in a while along with his friends. In those 10 years he never paid a visit to his hometown due to financial issues and decided not to get married anytime soon as he wanted to settle the financial issues his family was facing.
On presentation to our hospital:
He was obese with central obesity
His pulse rate was 100 bpm
Blood pressure - 110/70mmhg
RR - 21 cpm
Spo2 - 98% on Room Air
Temp - 98.6 %
GRBS - 151 mg/dl
GENERAL EXAMINATION:
He weighed 98 kgs and his abdominal girth measured 100 cm
He had no pallor, icterus, clubbing, cyanosis, lymphadenopathy
He had bilateral pitting type of pedal edema present upto his knees
JVP was raised
SYSTEMIC EXAMINATION:
CARDIOVASCULAR:
Inspection:
Shape of the chest - Ellipsoid
No dilated veins, scars, sinuses
No cutaneous lesions
No breast abnormalities
Palpation:
Apex beat palpated in 6th ICS 1 cm lateral to MCL
No palpable pulsations in aortic or pulmonary area or tricuspid area
No palpable pulsation
No palpable epigastric pulsations
No palpable pulsations in sternoclavicular area
Auscultation:
Muffled S1, S2 +
RESPIRATORY SYSTEM EXAMINATION:
Inspiratory crepitations in Bilateral in IAA, ISA
PER ABDOMEN:
soft
Non tender
No organomegaly
Bowel sounds +
CENTRAL NERVOUS SYSTEM EXAMINATION:
Normal
PROVISIONAL DIAGNOSIS:
HEART FAILURE SECONDARY TO
? VIRAL MYOCARDITIS
? ALCOHOLIC
REPORTS:
ECG:
His blood picture, renal and liver parameters were in within the normal range.
On routine investigations his HbA1c was found to be 8.4 %.
His Ultrasonography of abdomen revealed Grade 1 fatty liver (probably secondary to his alcohol intake), mild ascites, right moderate pleural effusion.
2DEcho was done which revealed that all the 4 chambers to be dilated with an ejection fraction of 27, global hypokinesia, severe MR, trivial AR, severe LV dysfunction with mild PAH, dilated IVC (2.3cm)
A diagnosis of HEART FAILURE WITH REDUCED EJECTION FRACTION - 27%
DENOVO DETECTED TYPE 2 DIABETES MELLITUS
TREAMENT ADVISED:
He was started on
1. Tab Lasix 80mg in the morning, 40mg in the afternoon and evening
2. Tab Isosorbide mononitrate 10mg twice a day
3. Tab Hydralazine 25mg
4. Tab Telma 40mg
5.Tab Metformin 500mg once a day
and was advised for fluid of less than 1 litre and salt restriction of less than 2grams/day
He was advised for a coronary angiogram for which he visited Hyderabad. CAG was performed on 24th of January 2020 which turned out to be normal and he was started on Tab Vymada 50mg and Tab Met XL 12.5mg
(Sacubitril 26 mg and Valsartan 24 mg) along with Tab Ecosprin AV (75/20)
On regular at home monitoring of blood glucose levels which were within the normal range, he stopped taking Tab Metformin.
On 14th March 2020 he paid a visit to our hospital with the similar complains and a review scan of 2DEcho was done which revealed end point septal separation distance to be increased and Tab Vymada was increased to 100mg.
On July 28th, 2020 he presented to our OPD with the complains of Dyspnea at rest since 5 days which apparently aggravates when the patient is in supine posture and he also complains of occasional cough with scanty mucoid, non blood tinged sputum especially while he is asleep. He says he developed bilateral pedal edema extending upto his knee over the past 4 days followed by abdominal distension.
Patient appears to have gained weight with abdominal girth measuring 116cm and he weighed 101 kg
He weighs 93 kgs now
He appeared to be in respiratory distress with a respiratory rate of 28 cycles per minute and his saturation was at 98 % on room air.
His heart was beating at 120 bpm with a blood pressure of 100/70mmhg.
He was afebrile.
He had Icterus
His JVP was raised
CVS:
On palpation: His apex beat was in 6th intercostal space, 1cm lateral to midclavicular line.
On auscultation, S1 S2 +
His lungs were clear on auscultation
His abdomen was soft to palpate and bowel sounds were heard.
CNS: Normal
ECG & CHEST X RAY PA VIEW:
HEMOGRAM:
Hb - 13g/dl
TLC - 7000 cells/cumm
Platelet count - 2.28 L/cumm
Complete Urine Examination:
showed no albumin, sugars, RBCs
2-4 Pus & epithelial cells
Renal Function Test:
Urea - 53 mg/dl
Creatinine - 1.4 mg/dl
Uric Acid - 9 mg/dl
Calcium - 9.6 mg/dl
Phosphorus - 3.3 mg/dl
Sodium - 133 mEq/L
Potassium - 4 mEq/L
Chloride - 98 mEq/L
Liver Function Test:
Total Bilirubin - 4.60 mg/dl
Direct Bilirubin - 2.42 mg/dl
AST - 56 IU/L
ALT - 44 IU/L
ALP - 129 IU/L
Total Proteins - 6.2 gm/dl
Albumin - 3.9 gm/dl
His 2Decho showed dilated chambers with global hypokinesia, ejection fraction of 26 %, severe MR, mild TR, Trivial AR, mild pericardial effusion, mild PAH and IVC measuring 1.7 cms.
Along with INJ LASIX 40MG TID
TAB VYMADA 100 MG BD
TAB VALSARTAN 80MG OD
TAB MET XL 12.5MG OD
TAB DYTOR PLUS 10/25 OD
THESIS
August 09, 2021
TITLE;
"LIVER FUNCTION TESTS IN TYPE II DIABETES MELLITUS IN RURAL TERITIARY CARE CENTRE”
INTRODUCTION:
Diabetes mellitus is a complex metabolic condition defined by level of hyperglycemia giving rise to micro vascular and macro vascular complications 1 .
Current estimates suggests that there are 170 million people suffering from DM worldwide and this number is going up to 266 million by 20302.The prevalence of DM in India is around 31 million and this number will increase to 80 million by 20302.
Indians develop diabetes at younger age, with lower degree of obesity and have increased risk of chronic diabetic complications. Hence DM is a major public concern in India. Various complications related to micro or macro vascular diseases like retinopathy, nephropathy, neuropathy, ischemic heart diseases and peripheral vascular disease have been reported. Liver diseases are often overlooked as a complication of DM.
Infact VERONA-DIABETES POPULATION BASED STUDY has shown that among patients with DM standardised mortality rate from cirrhosis was higher than cardiovascular diseases 3.Though association of diabetes with cirrhosis has been recognised for more than 100 years, liver diseases in diabetes remains under estimated 4.
Abnormal liver function test results are more common in diabetes mellitus than in the non-diabetic population as well as in patients with type 2 diabetes than in those with type 1 diabetes. Elevated activities of the two serum transaminases; alanine transaminase (ALT) and aspartate transaminase (AST) may be associated with liver disease. Elevation of these enzymes is strongly related to obesity, diabetes and dyslipidemia, and their measurement may act as a surrogate marker of NAFLD presence.
This study was conducted to estimate the prevalence of elevated liver transaminase levels among patients with type 2 diabetes and to determine the associated risk factors.
AIM:
To assess the pattern of liver function test in type 2 diabetes milletus.
OBJECTIVES:
To determine the liver function tests (serum bilirubin, AST, ALT, alkaline phosphatase) in patients with type II diabetes mellitus.
To determine the associated risk factors for abnormal liver function tests in patients with type II diabetes mellitus.
PATIENTS AND METHODS:
PLACE OF STUDY: Department of General medicine Kamineni Institute of Medical Sciences, Narketpally
STUDY PERIOD: October 2018-September 2020
STUDY DESIGN: Cross-sectional study
SAMPLE SIZE: 80
INCLUSION CRITERIA:
• Presence of type 2 diabetes Mellitus in patients above the age of 40 years
• Duration of type 2 diabetes Mellitus at least 1 year and above.
EXCLUSION CRITERIA:
1. Age less than 40 years.
2. Duration less than one year.
3. Consumption of alcohol.
4. Seropositivity of HbsAg and antiHCV antibody.
5. Seropositivity of HIV ELISA.
6. Patient on drugs proven to cause steatohepatitis (steroids, amiodarone, oral contraceptive pills, and other estrogen containing preparations).
7. Patients with renal failure and cardiac failure.
METHODOLOGY:
The study was approved by the ethics committee of Kamineni Institute of Medical Sciences, Narketpally.
All patients satisfying the inclusion criteria are enrolled in the study.
A written informed consent has been taken from the patients prior to the start of the study.
Measurement of height, weight, waist circumference, hip circumference and calculation of BMI and waist to hip ratio.
A total of 80 type 2 diabetic patients who met the inclusion criteria were studied during this period. Both inpatients and outpatients attending outpatient department were included in the study.
Body weight was taken while the patients barefooted and in light clothing, using a weighing scale with accuracy of ±100 g. Standing height was measured without shoes to the nearest cm with the shoulders in a relaxed position and the arms hanging freely. Body mass index. (BMI) (kg/m 2) was calculated as the ratio of weight (kilograms) to the square of height (meters). Patients' BMI was classified according to WHO classification, as being normal (BMI; 18.5 to 24.9 kg/m 2), overweight (BMI; 25 to 29.9 kg/m 2) or obese (BMI>30 kg/m 2).
Waist circumference and hip circumference was measured in a standing position using non stretchable tailor measuring tape to look for central obesity. Central obesity is defined in men by a waist-to-hip circumference ratio greater than 1.0 or a waist circumference greater than 40 inches (102 centimetres). In women, central obesity is defined by a waist-to-hip ratio greater than 0.8 or a waist circumference greater than 35 inches (88 centimetres).
All the above patients were examined and screened for HbsAg, anti-HCV antibody, HIV ELISA and were found to be negative. Morning samples of venous blood were collected from patients after fasting for at least 14 hours and tested for glucose, urea, Creatinine (using semi auto analyser Merck 300), haemoglobin A1C 35 (HbA1C) [Using High Performance Liquid Chromatography method], for the liver enzymes; ALT and AST [Using semi auto analyser Merck 300], and for lipid profile including total cholesterol (TC), high density lipoprotein (HDL), triglycerides (TGL), and low density lipoprotein (LDL)[ Using semi auto analyser Merck 300] and serum protein, albumin, globulin(Using calorimetry photochem -5). Elevated ALT and AST levels were defined as enzyme activity >40 U/L respectively, according to the clinical assay adopted by the centre‘s laboratory.
Ultrasound abdomen was done for all patients, to look for size of the liver, echogenicity of liver parenchyma, any evidence of chronic liver disease like coarse echo texture of liver, dilated portal vein and/or splenomegaly. The diagnosis of fatty liver was based on a diffuse hyperechoic echo texture (bright liver) and increased liver echo texture compared with the kidneys.
INVESTIGATIONS:
Complete blood picture
Complete urine examination
HbsAg
AntiHCV antibody
HIV ELISA
Blood sugar: FBS, PLBS
HbA1C
Blood urea
Serum Creatinine
Serum electrolytes
Liver function test
Serum bilirubin
Direct bilirubin
Indirect bilirubin
Aspartate transaminase
Alanine transaminase
Alkaline phosphatase
Serum total proteins
Albumin
Fasting Lipid Profile
Total cholesterol
HDL
LDL
VLDL
Triglycerides
Ultrasound abdomen
ECG
LINK TO COMPLETE THESIS WITH MASTER CHART
A 44 year old man presented with a 3-day history of bilaterally symmetrical rapidly progressive generalized edema.
Present Illness
An agile stonemason, the patient reported that this symptom first started suddenly 3 days ago, at night, when he noticed he started feeling facial puffiness with pedal edema. The next morning, while brushing his teeth, the patient noticed he had facial puffiness, in the mirror. At the same time, he also noticed that he developed bilaterally symmetric, pitting type pedal edema, extending upto the middle of his legs. He immediately presented to the hospital with these complaints.
On interviewing the patient further, he denied having breathlessness, palpitations or chest pain. He reported frothing of urine but no haematuria. He also reported gradually decreasing urine output over the past 3 days. He did not have pain during micturition, no pus or any other abnormal discharge (casts) in urine. He did not have any history of vomiting or diarrhea, no history of acute retention of urine, no prior history of fever or rash, no history of antibiotic usage or any drugs in the past 1 week. The patient also denied any history of yellowish discoloration of skin or sclera.
Prior to this, the patient reported that since 2011, he had severe joint pains, which were initially asymmetric and gradually became bilaterally symmetrical and involving the small joints of his hands and wrist. The joint pains were associated with significant local edema, and painful limitation of movements, which made his job (stonemasonry) difficult.
[Other activities which were painful and difficult for the patient were -
Holding his cup of tea or glass of water,
Pain in his finger joints and wrist while brushing,
Pain while holding mug when taking bath and
Pain in toes and ankles on both sides when walking)]
He reported that he also had debilitating early morning pains and limitation of movements in his hands, wrists and feet, which usually lasts for about an hour, He reported that the pains and limitation of movements improved with activity, with gradual reduction in edema of joints.
From 2011 to 2019, these joint symptoms gradually progressed in severity, now also involving several large joints (shoulders, elbows, knees and hips) warranting several medical consults, where he was frequently prescribed pain killers. The patient did not have any documentation of the pain killers he took in these 8 years. In December 2020, he presented to our hospital with similar complaints of joint pains, when he was prescribed with Etoricoxib and Febuxostat (he had hyperuricemia). He reported that his symptoms alleviated with these drugs but he intermittently had worsening of same symptoms in the interim. The patient denied any history of skin rash, photosensitivity, nasal or oral ulcers, chest pain or abdominal pain, weakness in his limbs (such as difficulty in taking stairs or lifting heavy stones and nor any weakness in his distal aspects of limbs such as mixing food, buttoning his shirt or holding a glass or slipping of footwear), isolated single joint pain or edema, or a past history of kidney stones. He also does not have any history of difficulty in swallowing, altered bowel habits, pain in the pulp of his digits, or painful tearing, photophobia or visual loss. He also denied any history of gritty sensation in eyes or dryness of mouth.
Apart from these, the patient reported that, for the past 3 days, he has burning sensation in his eyes with increased tearing but no visual deficits. He also reported for the past 1 year, he developed subcutaneous swellings in the proximal joints of his fingers. He denies any history of early satiety or post prandial fullness or pain. He reported that his clothes have slightly loosened over the past 1 year with involuntary weight loss and loss of appetite. He denies having a history of wrist or foot drop, chest pain, palpitations or breathlessness. No history of loss of consciousness, falls or tingling or numbness in his feet or hands.
Past History
No significant past history.
Medical/Surgical History
Chronic intermittent use of analgesics (type and dose unknown). Has been using Etoricoxib 60 mg and Febuxostat 80 mg intermittently for the past 8 months. No relevant surgical history. No history of allergy or atopy.
Personal History
The patient had been working as a stonemason for the past 20 years. He is a devout Catholic Christian and a strict teetotal (has never smoked or consumed alcohol in his life). He stays with his wife and 2 children (elder son and younger daughter) in Miriyalguda. He is from a close-knit family and regularly socialises with his family (parents and his 2 elder brothers). Apart from his troubling joint pains, he used to a have a fairly balanced and good quality of life, with good sleep every night, good appetite and adequate access to nutritious food and clean drinking water. He also had a balanced social well-being with a tightly-knit community at home and his church.
However, since the last 1 year, his appetite started to decrease and he also involuntarily lost weight. His bowel and bladder habits have always been normal but these joints pains have forced him into early voluntary retirement from his job in 2019. His and his family's finances have been supported by his brothers and from generous donations from his church. He feels his mental health has remained intact, thanks to his supportive family and fellow churchgoers.
Family History
No significant family history reported.
Social & Educational History
Married for 18 years with 2 children. Primary education upto Class 7 in Telugu medium.
Immunization History
None taken since birth.
Problem Representation / History Analysis
A 44 year old stonemason from Miriyalguda, presented with a 3 day history of anasarca, frothy urine and gradually decreasing urine output, on a background of a 10 year history of chronic bilaterally symmetric polyarthritis (evidenced by severe pain, edema and limitation of joint movements).
Localisation of Acute Problem
Anasarca and frothy urine with decreasing urine output suggest a renal pathology. Proteinuria causing anasarca likely due to glomerular pathology. Other systemic causes like heart failure and liver dysfunction can be ruled out due to absence of dyspnea, palpitations, bendopnea or syncope. Liver dysfunction can be ruled out by lack of jaundice, melaena or hematemesis (from bleeding varices), and abdominal distention not occurring prior to pedal edema
Within the kidney, pre-renal and post-renal causes can be effectively ruled out from the absence of volume loss (vomiting, diarrhea, diuretic abuse or burns) and no history of acute retention of urine or lower urinary tract symptoms (LUTS) like frequency, urgency, hesitancy or precipitancy. The presence of frothy urine and edema strongly supports a glomerular pathology due to significant loss of protein and also decreased urine output. Isolated defects in tubular/interstitium are unlikely as such patients have a deficit in maintaining urinary concentration, which causes polyuria. Such a high range of proteinuria causing anasarca is also not seen with tubular/interstitial pathologies alone.
Provisional Diagnosis - Acute Glomerulopathy (Glomerulonephritis / Nephrotic syndrome)
Features to look for -
1. Hypertension (secondary hypertension in Glomerulonephritis)
2. Haematuria on Urine Microscopy (particularly dysmorphic RBCs in urine)
3. Quantification of Proteinuria
4. Serum Albumin / Total Proteins
5. Urine specific gravity / calculated urine osmolality to check for isosthenuria (to look for secondary tubular/interstitial damage)
6. Renal biopsy, if diagnosis remains uncertain
Localisation of Chronic Problem
This 44 year old man has a 10 year history of bilaterally symmetrical progressive inflammatory polyarthritis. Features favouring an inflammatory pathology are -
1. Features of inflammation such as severe pain associated with edema of the joints and limitation of range of active movements
2. Early morning stiffness, lasting for more than 30 mins (for 1 hour in this patient)
3.Pain and edema of joints improving with activity and worsening with rest
4. Features of uncontrolled systemic inflammation such as fever, involuntary loss of weight associated with loss of appetite.
5. Swellings at joints and deformation of normal joint posture
Provisional Diagnosis - Bilaterally Symmetric Chronic Progressive Inflammatory Peripheral Polyarthritis
Clinical Examination
Initial examination revealed, the patient was conscious, coherent and co-operative, lying in bed in supine position. He was in some visibly apparent distress with flexion at his elbows and wrists, bilaterally, which were mildly painful when resting on the bed and his abdomen, respectively. The patient was dressed in a round neck t-shirt and when asked to sit up and take his t-shirt off, he had significant pain and limitation of movements at multiple joints but no weakness.
Vitals were taken in supine and sitting position -
Supine Position
Pulse - 92 bpm, regular, normal volume, condition of vessel wall - normal, no radio-radial or radio-femoral delay. All peripheral pulses were normal.
Blood Pressure - 140/90 mmHg
Temperature - 99.3F
Respiratory Rate - 24 cycles per minute. Mildly acidotic + (with prolonged duration of expiration)
Sitting Position
Pulse - 96 bpm, regular, normal volume, condition of vessel wall - normal, no radio-radial or radio-femoral delay.
Blood Pressure - 150/90 mmHg
Head to Toe General Examination
General Condition - Fair built and appears well nourished.
Hair - Thin and slightly greyed. Not easily pluckable or no areas of scarring or non-scarring hair loss. No lesions noted on the scalp.
Eyes - No conjunctival chemosis or injection, No redness or corneal lesions. Bilateral, purplish reticular markings noted on the sclera of both eyes. Palpebral conjunctival pallor +. No icterus. No cyanosis. Bilateral Periorbital puffiness +
| Periorbital Edema +. Pallor was also + |
General Head, Neck & ENT - No abnormalities. No lymph node enlargement.
Axial - No apparent spinal deformities
Fingers and Nails - Leukonychia +. No clubbing or cyanosis. Capillary refill time - 2 seconds.
Bilateral pitting type pedal edema +, extending upto middle of legs.
Systemic Examination
Musculo-Skeletal System
Inspection - No visibly apparent spinal deformities;
Palpation - Inspectory findings confirmed. No spine tenderness.
Movements - Atlanto-occipital - Flexion, extension and lateral flexion normal
Atlanto-axial - Rotation of head normal
Spinal Flexion, Spinal Extension, Lateral Flexion and Rotation are normal
Appendicular Skeleton - Upper Limbs (Positive Findings)
Shoulders (both sides) -
- Inspection - Attitude - Slightly flexed and internally rotated; Contour normal; No edema or erythema
- Palpation - Mild increase in temperature on both sides - Range of Movements - Mild Active and Passive limitation of all range of movements (flexion, extension, adduction, abduction, internal rotation and external rotation)
Elbows (both sides) -
- Inspection - Attitude - mid-flexion; alignment of elbow and forearm - normal; Edema +; No scars or sinuses; no muscle wasting
- Palpation - All Inspectory findings are confirmed; Raised temperature +; Edema +; Wincing on touch +; Fluctuation test +; 3-point bony relationship intact
- Range of Movements - Severe pain on active movements of flexion, extension; Mild pain with supination and pronation;
Wrists (both sides) -
- Inspection - Attitude - Mild extension; Radial deviation of wrists +; Diffuse edema +; Redness +;
- Palpation - All Inspectory findings confirmed; Temperature raise +; Wincing on touch +;
- Range of Movements - Severely limited and extremely painful active movements of flexion, extension, radial deviation and ulnar deviation.
Hands (both sides) -
- Inspection - Attitude - Palmar subluxation and Ulnar deviation of the MCP joints; Swollen and Erythematous PIP joints; No swelling or redness of DIP joints; No apparent muscle wasting; Mild hyper-extension of PIP of thumbs; Pulp of fingers normal
- Palpation - All Inspectory findings are confirmed; Temperature raise +; Wincing on gentle palpation of MCP joints and PIP joints; Palpation of DIP joints is normal; Swellings also + on 3rd and 4th PIP joints on both sides. Z-deformity +.
- Range of Movements - Severe pain and severe limitation of active movements of flexion, extension and ulnar and radial deviation of MCP joints; severe pain and limitation of active and passive movements of flexion and extension at PIP joints. DIP joints normal.
Appendicular Skeleton - Lower Limbs (Positive Findings only)
Hip Joints (both sides)
- Limitation of passive movements of flexion and extension (towards the end of range of motion);
Knee Joints (both sides)
- Inspection - Swelling and erythema +; Attitude - flexion;
- Palpation - All Inspectory findings are confirmed; Raised temperature + ;
- Range of movements - Severe pain and limitation of active and passive movements of flexion and extension and lateral and medial rotation; (Patient was unable to stand on Day 1 and was able to stand on Day 2 with analgesic use).
Ankles (both sides)
- Mild pain and limitation of active and passive movements of plantar flexion and dorsiflexion; Mild pain and limitation of movements of inversion and eversion.
- Palpation of Achilles tendon is normal.
Foot examination (both sides)
- Mild pain and limitation of passive movements of flexion and extension of MTP joints; great toe flexion and extension normal;
Other Systems Examination
Cardiovascular System - No abnormalities detected
Respiratory System - No abnormalities detected
Abdominal Exam - No abnormalities detected
Nervous System - No deficits detected
Investigations
 |
| X-ray AP view of the hands and wrists - Osteopenia and erosions of the MCP and PIP joints are noted. Scallop sign +. Significant soft tissue swelling is also noted. |
 |
| Chest X-ray PA view - Full inspiratory, underexposed film with no malrotation or angulation. Bones - Clavicle, Head of Humerus, Coracoid process and acromion of scapula appear normal. The ribs are normal. No mediastinal lymph nodes or enlargement. The right heart border shows mildly dilated right atrium. The left heart border shows a prominent aortic knuckle, the pulmonary bay area is normal, the left atrial appendage appears normal and the left ventricular free wall also appears normal. The bronchovascular markings are also prominent, likely due to underexposure. |
 |
| Standard 12 lead ECG with normal voltage and speed @ 25mm/s; P waves, QRS complexes and T waves have normal morphology and duration; P-P and R-R intervals are normal. PR and QTc intervals are normal. |
 |
| Current Admission - Blood tests |
 |
| Blood work from previous presentations to hospital. RA factor was negative 24hrs urinary protein: 1500 mg 24hrs urinary creatinine: 0.8 |
 |
| Urine Microscopy - Freshly voided urine sample was centrifuged at high speed (> 2700 RPM) and sediment collected and fixed on glass slide and examined under microscope at 400 (10x * 40x) showed DYSMORPHIC RBCs (black circles) and occasional pus cells (red circles). Dysmorphic RBCs were those that had altered shape, microcytic or with membrane defects. |
With a provisional diagnosis of Acute Glomerulopathy on the background of bilaterally symmetric chronic progressive erosive peripheral polyarthritis, features supporting the diagnosis of glomerulonephritis were -
- Secondary Hypertension
- Oliguria (360 ml urine in the last 24 hours)
- Hypoalbuminemia (Serum Albumin 2.5g/dl) and Anasarca
- Dysmorphic RBCs in Urine
(A review of literature was done to evaluate the sensitivity and specificity of dysmorphic RBCs for glomerular disease pathologies - One study conducted in Bangladesh showed that urinary dysmorphic RBCs were 92.7% sensitive and 100% specific for a biopsy confirmed diagnosis of glomerulonephritis. [1]
Similar values of sensitivity and specificity was also confirmed in another study jointly conducted in Australia and China, where glomerulonephritis was confirmed with renal biopsy. [2])
Thus, with glomerular disease being most likely, an anatomical diagnosis is made. The etiological cause for glomerular injury needs to be ascertained.
A careful construction of the problem representation for this patient and insight into the sequence of his life events can provide clues that the current acute problem could be a sequelae of his long term, poorly treated chronic problem.
Thus, a good clinical diagnosis of his musculo-skeletal problems is required to get a better picture of his current illness.
The patient has Bilaterally Symmetrical Chronic Progressive Erosive Peripheral Polyarthritis. Differential diagnosis for such conditions include -
1. Rheumatoid Arthritis (most likely)
2. Rheumatoid Arthritis with coexistent Gout
3. Psoriatic Arthritis
4. Enteropathic Arthritis
5. Reactive Arthritis
6. SLE
7. Polymyositis / MCTD (Mixed Connective Tissue Disorder) (least likely)
With Rheumatoid Arthritis being most likely, ACR/EULAR classification criteria can be applied for diagnosis -
 |
| This patient has >10 joints involved with multiple small joints involvement - 5 points; Symptom duration 10 years - 1 point; RA Factor - NEGATIVE; CRP elevated & ESR - 120 mm/hr - 1 point; Total Score - 7/10 [3] Thus, a diagnosis of Rheumatoid Arthritis is likely. The clinical utility of RA factor came into question. A review of literature showed that sensitivity of RA factor for Rheumatoid Arthritis was 28% and specificity was 87%. For non RA rheumatological disorders, the sensitivity was 29% and the specificity was 88% [4]. Thus, the authors concluded that (due to high specificity and NPV), the test is best ordered when the suspicion for a rheumatological is low but just high enough, that a negative result would increase the post-test probability of a rheumatological disorder being unlikely. This patient had a chronic history of symmetric small joint and then large joint inflammatory peripheral polyarthritis, With minor erosions notable in the PIP and MCP joints of both hands, classification criteria are diagnostic for Rheumatoid Arthritis. No history of skin rash (psoriatic arthritis) or chronically altered bowl habits (enteropathic arthritis); No history of dysuria or burning pain during micturition or a history of severe burning pain in eyes with photophobia and excessive tearing or discharge (reactive arthritis) makes the other diagnoses unlikely. Epidemiologically, SLE occurs more commonly in females at a ratio of 9:1, coupled with this, the absence of other features of SLE, such as alopecia, photosensitivity rash, nasal or oral ulcers, serositis, hemolytic anemia etc. makes this diagnosis very unlikely. The absence of muscle weakness, muscle pain and the presence of destructive arthritis makes Polymyositis / MCTD extremely unlikely (Polymyositis usually causes nonerosive arthritis). Thus the current acute glomerulonephritis can be framed in the background of Chronic Poorly Treated Rheumatoid Arthritis. 4 scenarios are possible - 1. Poorly treated RA causing Secondary Amyloidosis (most likely) Secondary amyloidosis is most commonly seen in chronic poorly treated systemic inflammatory syndromes. This study shows that secondary amyloidosis is the most common cause of rapidly progressive glomerulonephritis in patients who were untreated for more than 10 years. [4] Coupled with features of amyloidosis of the heart, this is the most likely cause of his renal dysfunction. 2. Vasculitic Glomerulonephritis (IgA Mediated) The incidence of IgA nephropathy in patients with RA is similar to that in the general population. [5] 3. Primary Glomerulonephritis (Idiopathic) These include Mesangial / Mesangio-proliferative glomerulonephritis; Membranous Nephropathy; FSGS [6] 4. Renal Dysfunction secondary to drug use (less likely) Most commonly implicated drugs causing nephritic/nephrotic syndrome are Gold and Pencillamine, neither of which the patient used. The patient had chronic intermittent use of Etoricoxib but NSAIDS usually cause Tubulo-interstitial nephritis and not nephrotic syndrome. 5. Crystal Nephropathy (less likely) Gout crystals precipitate at a pH of 7.0 and often precipitated in the collecting ducts in the medulla, causing Acute Tubular Necrosis with little interstitial or glomerular involvement. Final Diagnosis - A 44 year old, who presented with a 3 day history of anasarca and decreased urine output is diagnosed with -Acute Glomerulonephritis, likely due to Secondary Amyloidosis due to Chronic Poorly Treated Seronegative Erosive Rheumatoid Arthritis. Dilutional Hyponatremia secondary to Anasarca due to Glomerulonephritis Hyperuricemia likely due to decreased Uric Acid Excretion Precipitating Gouty Arthritis Anemia of Chronic Disease secondary to Poorly Treated Rheumatoid Arthritis. Further PlanAbdominal Fat Pad Biopsy for Amyloidosis Needle Aspiration of Synovial Fluid for Crystal Induced Arthritis (Gout) Treatment
Pedagogic Questions
The clinical data and biopsy results of 194 SA patients who were treated in Peking Union Medical College Hospital from January 2009 to June 2015 were retrospectively analyzed. Results The highest sensitivity was achieved by biopsy of affected organs, with renal biopsy 97.4%, heart biopsy 95.0% and liver biopsy 87.5%. Among non-invasive biopsy methods, tongue biopsy was found to be 75% sensitive, followed by gingiva biopsy at 57%, abdominal fat pad aspiration at 57%, rectum biopsy at 16%, and bone marrow examination at 8%. Combination of tongue and abdominal fat pad biopsy yielded a detection rate of 93.1%. Conclusions Biopsy of the involved organ has the highest sensitivity. However, combination of multiple non-invasive biopsy methods may has sensitivity comparable to organ biopsy and is safer and more convenient. [7] 2. Single DMARD vs Combination therapy ? A Cochrane review, published in The BMJ [8] looked at the clinical efficacy of Methotrexate monotherapy vs Combination therapy (MTX + Non-biological or MTX + Biologicals). Data of Methotrexate -naïve patients was gleaned from this meta-analysis - Outcomes - The major outcomes of the review were American College of Rheumatology (ACR) 50 response, a composite measure of improvement in disease activity (dichotomous outcome); radiographic progression, measured by Larsen, Sharp, or modified Larsen/Sharp scores (continuous outcome); and withdrawals due to adverse events, including death (dichotomous outcome).    3. When to initiate dialysis? How long can we wait? Ex tempore interpretation of the AKIKI-2 trial. [9] 4. Can Rheumatoid Arthritis and Gout co-exist together? The study population included 813 patients, 537 (66%) were rheumatoid factor positive; 33% had rheumatoid nodules, and 53% had erosive joint disease. During 9771 total person-years of follow-up (mean 12.0 years per RA patient), 22 patients developed gout by clinical criteria. The great toe was the most common site of gout (12 of 22 patients). The 25 year cumulative incidence of gout diagnosed by clinical criteria was 5.3%. Typical intracellular monosodium urate crystals were present in 9 of 22 patients with acute gout; all had developed gout after the RA incidence date. The 25 year cumulative incidence of gout diagnosed by clinical criteria including presence of urate crystals is 1.3%. The prevalence of gout in RA on Jan 1, 2008 was 1.9% (11 of 582 patients) as opposed to expected prevalence of 5.2% (or 30 patients) based on National Health and Nutrition Examination Survey (NHANES) data using age and sex specific prevalence rates. [10] 5. Efficacy of Febuxostat vs Allopurinol for Gout ?  [11] |
- Sultana T, Sultana T, Rahman MQ, Rahman F, Islam MS, Ahmed AN. Value of dysmorphic red cells and G1 cells by phase contrast microscopy in the diagnosis of glomerular diseases. Mymensingh Med J. 2011 Jan;20(1):71-7. PMID: 21240166.
- Pollock C, Liu PL, Györy AZ, Grigg R, Gallery ED, Caterson R, Ibels L, Mahony J, Waugh D. Dysmorphism of urinary red blood cells--value in diagnosis. Kidney Int. 1989 Dec;36(6):1045-9. doi: 10.1038/ki.1989.299. PMID: 2689749.
- https://www.eular.org/myUploadData/files/RA%20Class%20Slides%20ACR_Web.pdf.
- Helin H, Korpela M, Mustonen J, et al. Renal biopsy findings and clinicopathologic correlations in rheumatoid arthritis. Arthritis Rheum 1995;38(2):242–7.
- Korpela M, Mustonen J, Helin H, et al. Immunological comparison of patients with rheumatoid arthritis with and without nephropathy. Ann Rheum Dis 1990;49(4): 214–8.
- Horak P, Smrzova A, Krejci K, et al. Renal manifestations of rheumatic diseases. A review. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2013;157(2):98–104.
- Zhang CL, Feng J, Cao XX, Zhang CL, Shen KN, Huang XF, Zhang L, Zhou DB, Li J. Selection of Biopsy Site for Patients with Systematic Amyloidosis. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2016 Dec 20;38(6):706-709. doi: 10.3881/j.issn.1000-503X.2016.06.013. PMID: 28065238.
- Hazlewood GS, Barnabe C, Tomlinson G, Marshall D, Devoe DJ, Bombardier C. Methotrexate monotherapy and methotrexate combination therapy with traditional and biologic disease modifying anti‐rheumatic drugs for rheumatoid arthritis: A network meta‐analysis. Cochrane Database of Systematic Reviews. 2016(8).
- Gaudry S, Hajage D, Martin-Lefevre L, Louis G, Moschietto S, Titeca-Beauport D, La Combe B, Pons B, De Prost N, Besset S, Combes A. The Artificial Kidney Initiation in Kidney Injury 2 (AKIKI2): study protocol for a randomized controlled trial. Trials. 2019 Dec;20(1):1-0.
- Jebakumar A, Crowson C, Udayakumar D, Matteson E. Co-Existence of Gout in Rheumatoid Arthritis: It Does Happen! A Population Based Study.: 134. Arthritis & Rheumatism. 2012 Oct;64.
- Huang X, Du H, Gu J, Zhao D, Jiang L, Li X, Zuo X, Liu Y, Li Z, Li X, Zhu P. An allopurinol‐controlled, multicenter, randomized, double‐blind, parallel between‐group, comparative study of febuxostat in C hinese patients with gout and hyperuricemia. International journal of rheumatic diseases. 2014 Jul;17(6):679-86.
SHORT CASE-1:
CASE PRESENTATION
History taken from Patient and Attendant (elder brother); Reliability 9/10.
A 49 year old English and Telugu language lecturer presented with a 2 month history of progressive asymmetric involuntary movements of his right index and middle fingers
Present Illness
The patient reports that he first noticed them happening nearly 6 months ago, which was very small in amplitude, affecting these two fingers only. He says that these movements often worsened with rest and abated with activity. They were not troublesome initially but for the past 2 months he has been unable to correct answer sheets because of the involvement of his thumb and maintaining stability of his hand was proving difficult. He describes these movements as involuntary, rhythmic to and from oscillations.
He also adds that his handwriting has become ugly with very small letters. On interviewing further, the patient reports that he feels stiffness in his wrists (Right>Left), which has now ascended to his elbows. He says the stiffness is present throughout the range of motion. He also says that since the last 1 month, the same involuntary movements also started appearing in his left hand.
At this point, he also says that his walking has become difficult with small, short steps and a forward stoop, and he feels that although he weighs 60 kgs. he feels like it weighs 100 kgs.
He does not report any difficulty in reading the newspaper, holding the paper, turning pages or folding it back. He does not have any difficulty in brushing his teeth or combing his hair. He also denies having difficulty in holding objects, such as holding a water bottle to drink nor any difficulty in mixing food and eating it. He does not have any difficulty in wearing a vest or in buttoning or unbuttoning his shirt. No difficulty in lifting his lower limbs and wearing a trouser.
The interview continues and we question for any difficulty in taking the stairs - he reports that he has been having difficulty in taking stairs up, in that he feels he sometimes might lose balance. He has no difficulty in descending stairs. The patient also denies having swaying of his trunk while walking or overshooting his hand while picking up objects.
On pressing further - he reports that he hasn't been having morning erections since 2 months and also reports a loss of sexual desire. He also says that since 2 months his bowel habits have been incredibly erratic, in that he sometimes has an immediate urge to defecate when he has tea and sometimes goes 2 to 3 days with constipation.
He, however, denies feeling dizzy or lightheaded when waking up in the morning. He denies having stiffness in his lower limbs, denies cotton wool sensation of floor, denies burning pain or inability to feel hot or cold stimuli. He also denies buckling of knees but, however, he reports that he has been having a great difficulty to walk in the dark since 2 months and says that he feels like he would definitely fall without support.
His brother gives a positive affirmation for all his symptoms and also says that he previously used to be a fairly jovial and hardworking man with good oratory skills, however, since the last 2 months he says his brother's speech lacks that 'edge' which he previously had. On asking further, the brother says that he has been speaking in a monotonous drab since 2 months.
The patient and his brother deny noting any fluctuations in his alertness, apathy or emotional instability to family or personal issues, no history of visual hallucinations, no history of incoherence of speech or irrelevant talk and no history of difficulty in managing finances or poor self care.
The patient denies ever having urinary incontinence, memory deficits, the brother vehemently denies the patient ever being anti-social, he does not have any difficulty in forming new memories or any visual deficits.
Past History
No similar complaints in the past. No history of Diabetes, Hypertension, Coronary Artery Disease, Seizures, Asthma or Tuberculosis.
Medical/Surgical History
The patient is not on any medications. He also did not report usage of any herbal or alternative medicine. He has no past surgical history.
Personal History
The patient is a teacher; he teaches English and Telugu for B.com and B.sc students in a college in Miriyalguda. He has been in this profession for the last 9 years. He has a triple M.A. in English, Sanskrit and Telugu.
The patient neither smokes nor drinks, he had a fairly routine lifestyle with waking up early in the morning and getting ready for his job. However since the lockdown, he had to stay at home with his college shut. He spends most of his time reading the newspaper and other literature. He lives with his wife and one son, who is studying Inter 2nd year. His sleep habits are well maintained. However, his bowel habits have changed in the last 2 months as detailed above. His appetite is good, he consumes vegetarian food on most days with a good access to nutritious food and clean drinking water. He occasionally enjoys non vegetarian food. He socialises well with his extended family and his local community. He is well respected among his peers and students alike.
Family History
No significant family history reported.
Social & Educational History
Married for 24 years with 1 child. Triple degree in MA in English, Sanskrit and Telugu.
Immunization History
Complete upto age 5.
General Examination
Patient is conscious, coherent & cooperative.
Vitals at the time of history taking -
PR - 88 bpm
BP - 190/110 mm Hg
After standing for 3 mins - BP - 160/110 mm Hg
Temp - Afebrile
RR - 16 cpm
No signs of Pallor, Icterus, Cyanosis, Clubbing, Generalized lymphadenopathy or edema.
Nervous System Examination.
Higher Mental Functions
1. Level of consciousness - Normal (CGS15/15)
2. Attention - Intact.
3. Orientation - to time, place and person - Intact
4. Language - fluency & latency, comprehension, repetition, naming, reading and writing - Intact. Prosody - impaired
5. Memory - immediate recall, recent and remote - Intact
6. Other higher mental functions - general knowledge, abstraction, judgement, insight and reasoning - Intact.
MMSE
29/30 (No cognitive impairment)
CN Examination
1st
Normal (smell of soap).
2nd
Counting fingers at 6mts both eyes normal.
3rd,4th,6th
Pupil size. N N
DLR/CLR. N. N
No pstosis, nystagmus.
5th
Both sensory & motor normal.
Corneal & Conjunctival reflex +.
7th
Nasolabial fold normal.
No deviation of mouth.
Salivation & Lacrimation unaffected.
8th
Rinne's AC>BC.
Weber's - No lateralization.
9 th, 10th &
Palatal movements normal.
No difficulty in swallowing.
Gag reflex present.
11th
Movements of neck in all directions+.
Lifting of shoulders +.
12th
Tone of tongue - Normal.
No wasting, no fibrillations & deviation of tongue.
Tongue tremor+.
MOTOR SYSTEM
Right. Left
✓Bulk Normal Normal
✓Tone
Upper limb R. L
Shoulder Normal Normal
Elbow Normal Normal
Wrist Hypertonia Normal
(Cog wheel rigidity)
Lower limb Normal Normal
✓Power
UL
Proximal 5/5 5/5
Distal 5/5 5/5
LL
Proximal 4/5 4/5
Distal 5/5 5/5
✓Reflexes
Superficial reflexes
Right Left
Corneal + +
Conjunctival + -
Abdominal + -
Plantar - -
Deep tendon reflexes
Right Left
Biceps 2+ 2+
Triceps 2+ 1+
Supinator 1+ Absent
Knee 3+ 3+
Ankle 1+ 1+
Clonus Absent. Absent
Involuntary movements - Resting tremors of Right upper limb 3-4Hz, high amplitude.
Gait - Reduced arm swing.
Finger tap and toe tap - Normal.
No decrease in speed on repeating the movement continuously.
✓SENSORY SYSTEM
Right Left
Pain + +
Fine touch + +
Temperature + +
Vibration
Medial malleolus 5.7s 4.6s
Patella 9s 4.3s
Elbow 4.8s 6.4s
Wrist 5s 7s
Proprioception Normal Normal
Stereognosis Normal
✓CEREBELLUM
Titubation - absent
HINTS
Head Impulse - negative
Nystagmus - negative
Test for skew - negative
Gait Ataxia absent.
Dysarthria absent.
Rebound phenomenon absent.
Intentional tremors - absent.
Pendular knee jerk - absent.
Tandem walking normal.
Coordination tests
Dysdiadochokinesia absent
Finger nose test normal
Heel knee test normal
Rombergs Test - Negative
Micrographia +
✓This is a test to elicit the bradykinesia component of Parkinson's disease.
✓Findings - The movements in the right lower limb is slower than the movements in the left lower limb.
✓The first test was only toe tapping, the second test is entire foot tapping.
Rapid supination and pronation - Diadochokinesia
✓MENINGEAL SIGNS
Neck stiffness - Absent
Kernig's sign - Negative
Brudzinski's sign - Negative
✓AUTONOMIC
Postural hypotension+(Supine - 180/110, Standing 160/90).
Resting tachycardia absent(PR 80/min, regular)
Abnormal sweating absent.
H/O erectile dysfunction+.
Cardiovascular System
S1, S2 +.
Apex beat in 5th ICS on the MCL.
JVP normal.
ECG
✓ Shows Sinus Tachycardia with pseudo infarct pattern in leads I and aVL with dagger q waves in the same leads.
✓ No late intrinsicoid deflection of R wave with modified Cornell criteria showing LVH.
2 D Echo
✓ Grade II diastolic dysfunction.
Respiratory System
Shape & symmetry of chest - Normal
Respiratory movements - Equal on both sides
BAE+
NVBS
Abdominal Examination
Soft, Non-tender
No organomegaly
Bowel sounds+
Problem Representation -
A middle aged man presenting with a 6 months history of gradually progressive, asymmetric rest tremor with autonomic features is provisionally diagnosed with
1. Idiopathic Parkinson's Disease Stage 1 with denovo HTN.
2. Multiple System Atrophy - Parkinsonian Type (MSA-P).
Treatment
1. Tab. Syndopa Plus 125 mg QID
2. Tab. Syndopa 125 mg CR OD
3. Tab. Telma 40 mg O
Sourced From - Resting Tremor (sravyakandala.blogspot.com)
SHORT CASE-2:
19 year old male resident of Nalgonda and currently studying intermediate, came to OPD with complaints of:
-Itchy Ring leisons over arms, abdomen, thigh and groin since 1 and half year.
-Purple stretch marks all over abdomen, lower back, upper limbs, thighs since 1 year.
-Abdominal distension and facial puffiness since 6 months.
- Pedal edema since 3 months.
- Low back ache since 3 months.
- Feeling low, not feeling to talk to anyone.
- Weight gain and decreased libido since 3months.
- Loss of libido and erectile dysfunction since 2 months.
Pt was apparently alright one and half year ago, when he slowly developed erythematous round leisons which are annular shaped and itchy all over abdomen, upper limb, groin and inner thigh region.
No history of fever back then. No other complaints apart from skin lesions.
Pt visited local RMP where he prescribed auyurvedic medications and other creams ( unknown composition as pt don't have them currently). He also prescribed tablets (unknown composition). Patient started using all these medications for 1-2 months.
Leisons reduced a bit after using medications.
Later after 2 months he developed multiple hyper pigmented plaques over lower limbs abdomen, for which he again visited same place and used ayurvedic oils over the leisons.
He also used clobetasol ointment over the leisons. (for approximately 1 year all over the body)
He started noticing pink striae over his abdomen first and later on back and over arms, which were gradually increasing in size.
Later he visited a hospital and used miconazole and luliconazole ointments also.
He used clobetasol ointment all over the leisons for long time.
He started noticing abdominal distension and facial puffiness, weight gain, but never visited any hospital.
Later he developed pedal edema and low back ache since 3 months .
His consulted a dermatologist at this point of time who advised to consult physician and prescribed monteleukast, itraconazole tablets, luliconazole ointment for tenia corporis.
He stopped all medications one month ago and visited our opd with complaints of pink striae and easy fatigue, weakness and low back ache.
His brother also gave history of pt being moody and feeling of low self esteem due to multiple leisons.
He even complaints pt wouldn't step out of house and always stays indoor and wouldn't interact with others.
No complaints of chest pain, sob, palpitations.
No complaints of decreased or frothy urine.
No other negative history.
No h/o DM, HTN, TB, ASTHMA, CAD.
ALLERGIC HISTORY - pt gives h/o allergy to eggs, brinjal.
O/E: Pt was c/c/c
BP - 160/100 mmHg
Pr - 96 BPM, regular ,normovolemic .
Rr - 18/min
Spo2- 98% on ra.
Weight - 63 kg.
Height - 175 cm.
GENERAL EXAMINATION:
NO pallor, icterus, cyanosis, clubbing, lymphadenopathy.
Pedal edema present - pitting type extending upto knee.
Abdominal distension present.
Moon face present
Pink striae noted over anterior abdominal wall and on low back and on upper arms and thighs.
Thin skin present.
Poor healing noticed over leg ulcers and easy bruising noted.
Acne present over face.
Acanthosis nigrans noted over neck.
GYNECOMASTIA PRESENT.
Buffalo hump present.
Sparse scalp hair.
Skin examination - Multiple itchy erythematous annular leisons noted all over abdomen, upper limb, groin and inner thigh region.
Multiple hyperpigmented plaques noted over bilateral lower limbs.
SYSTEMIC EXAMINATION:
CVS - S1S2 heard. No murmurs
RS - BAE present.
No adventitious sounds.
P/A - Soft, distended.
No organomegaly.
Bowel sounds present.
CNS - HMF - INTACT R. L
MOTOR SYSTEM - POWER - UL 5/5 5/5
LL 5/5 5/5
Proximal muscles lower limb - power is 4/5.
TONE - NORMAL.
REFLEXES - B. T. S. K. A. P
R. +2 +2. +1. +2. +1. FELXOR
L. +2. +2. +2. +2. +1. FLEXOR.
CRANIAL NERVES - NORMAL.
Difficulty in getting up from chair was noticed.
PROVISIONAL DIAGNOSIS -
? IATROGENIC CUSHINGS SYNDROME .
TINEA CORPORIS.
DENOVO HTN .
INVESTIGATIONS:
CBP - HB - 13.4 g/dl
TLC - 6,800
PLT - 1.5 lakhs.
RBS - 139 mg/dl
CUE - ALBUMIN - +1
SUGARS - NIL.
PUS CELLS - 3-4
RBC - NIL.
LFT - TB -1.03
DB-0.21
ALBUMIN - 3.9
RFT - UREA - 22
SERUM CREATININE -0.6
ELECTROLYTES - NA - 136
K- 4
CL-98
USG ABDOMEN - NORMAL.
ECG - SINUS TACHYCARDIA
LVH PRESENT.
This was picture of striae one year ago when it gradually started:
On presentation to opd pictures: 28/05/21
We took dermatologist opinion for tenia corporis where they advised
Ointment AMLORFINE
FUSIDIC ACID CREAM.
SALINE COMPRESS OVER LEISONS.
Plan to start anti fungals on next visit once dose of steroids is reduced .
OPTHAL opinion Was taken to look for visual acuity and cataract.
No features of lens opacities noted.
BUT IOP was high, where they advised to follow up.
We advised pt to get fasting 8am serum cortisol levels and was planned to start on low dose steroids to avoid adrenal crisis.
8AM S CORTISOL LEVELS (30/5/21)
- 0.46 mcg/dl (very low).
(normal range - 4.3-22.4 mcg/dl).
In view of lvh pt was started on tab telma 20 mg od.
On 3/6/21 - ACTH STIMULATION TEST WAS DONE.
BY INJECTING 0.4 ML OF ACTOM PROLONGATUM INJECTION (ACTH) INTRA MUSCULAR @ 7am
1 HR LATER FASTING SERUM CORTISOL SAMPLE WAS SENT.
VALUE - 0.73 mcg/dl
Indicating there was HPA AXIS suppression and pt was started on TAB HIZONE 15 mg per day in three divided doses @ 8am ,12 pm and 4 pm.
Pt was asked to follow up after one month .
ON NEXT VISIT: (25/6/21).
Pt was symptomatically better, pedal edema subsided.
Striae were pale in color and we're subsiding.
Weight - 67kg
Ht -175 cm.
Bp- 160/100 mmHg.
Pr -88bpm.
Dose of Tab hizone was reduced to 10 mg per day in divided doses for one month.
In view of low back ache Xray LS spine was done which was normal and pt was advised.:
Tab Shelcal 500 OD and Tab Vit D 3 Od.
Tab ULTRACET /PO/SOS.
Psychiatry opinion was taken and he was diagnosed with moderate depression.
In July 2021 pt was complaining of fever, sore throat and dry cough since 3 days and he was tested positive for COVID 19, we advised him home isolation and PCM 650 Mg /po /sos .
He was advised to continue tab hizone tablets as it was advised.
He recovered within one week.
Next visit: (6/8/21).
BP- 170/100 - TELMA DOSE WAS INCREASED TO 40 MG OD.
PR - 88bpm. regular, normovolemic.
Wt- 69 kg
Height -
Abdominal girth - 96cm
Pt complaints of excoriation over striae and appearance of erythematous macules over abdomen whenever he takes food he is allergic to.
Took dermatologist opinion for it. They started him on Tab Itraconazole 100 mg bd. And lulifin cream and tab levocitrixine 5mg od.
His brother complaints of depressed mood, pt not going out due to social stigma. Psychiatric counselling was given.
He still complaints of low back ache.othropedics opinion was taken and advised to continue Ultracet and tab Shelcal .
Cbp , cue and electoltes were repeated which were all in normal range.
USG ABDOMEN was done - Normal kidney size bilateral and CMD maintained. No other sonological abnormality noted.
As his lesions dint subside we reduced dose of hisone to 7.5 mg per day, to see response.
At this point of time we are now in diagnostic dilemma whether endogenous CUSHINGS is also present in this patient, as he is responding slowly to treatment.
We advised him to review after 15 days to see progress . And accordingly plan to evaluate further to rule out endogenous CUSHINGS SYNDROME.
FINAL DIAGNOSIS:
IATROGENIC CUSHINGS SYNDROME SECONDARY TO TOPICAL CLOBETASOL APPLICATION ALL OVER BODY FOR APPROXIMATELY ONE YEAR.
TINEA CORPORIS
DENOVO HTN.
THESIS
AUGUST 09, 2021
TITLE
“ASYMPTOMATIC LEFT VENTRICULAR (LV) DIASTOLIC DYSFUNCTION IN PATIENTS OF TYPE 2 DIABETES MELLITUS OF 1 TO 10 YEARS DURATION”
INTRODUCTION
In the year 2000, India topped the world with the highest number of people with Diabetes Mellitus with 31.7 million people affected with it, giving it a status of a potential epidemic. [1] In 2014, this figure more than doubled to 62 million of the adult population diagnosed with Diabetes. According to Wild et. al. this figure may reach nearly 80 million by the end of 2030,
further establishing its status as a potential epidemic. [2] According to the recently conducted National Family Health Survey,
(NFHS-4, 2015-16) 6.3% of adult women in Nalgonda suffer from Diabetes Mellitus, with Khammam having the highest prevalence at 7.6% of its adult population. [3] Left ventricular diastolic dysfunction in asymptomatic patients with diabetes mellitus may represent the early stage of diabetic cardiomyopathy even in patients without structural cardiac disease or systemic hypertension and have a preserved left ventricular systolic function. [4] Diabetic cardiomyopathy was first reported by Rubler et al. [5] in 1972 when they described four diabetic patients with heart failure, normal coronary arteries, and without obvious aetiology for heart failure and stated that it was due to diabetic cardiomyopathy.
Studies have reported a high prevalence of pre-clinical LV diastolic impairment in diabetic patients [6] and this cardiac complication may represent the reversible early stage of heart failure which is termed diabetic cardiomyopathy. Cardiac involvement in patients with diabetes mellitus may occur relatively early in the course of disease, impairing left ventricular (LV) relaxation (diastolic dysfunction) and later on can affect ventricular contraction (systolic dysfunction). [6]
AIM
To Study Asymptomatic Left Ventricular (LV) diastolic dysfunction in patients of Type 2 Diabetes Mellitus of 1 to 10 years duration.
OBJECTIVES
To study asymptomatic diastolic dysfunction in patients with Type 2 Diabetes Mellitus.
RESEARCH QUESTIONS
1. Is there a correlation between glycaemic control and grade of diastolic dysfunction?
2. Does duration alone affect the grade of diastolic dysfunction?
3. Does grade 3 diastolic dysfunction (restrictive filling pattern) occur in diabetics of less than 10 years duration?
METHODOLOGY – PATIENTS AND METHODS
PATIENTS: Type 2 Diabetes Mellitus patients (insulin dependent or non-dependent), that are free from cardiac symptoms (e.g., exertional Dyspnea, Angina) with duration between 1-10 years, of out-patients or in-patients admitted in Medical wards or ICU in KIMS, Narketpally.
✓ STUDY DURATION: Recruitment of patients would begin from
October 2018 - September 2020.
✓ STUDY DESIGN: Qualitative, Cross-sectional, Exploratory
✓ SAMPLE SIZE: 60
✓ INSTITUITIONAL ETHICAL COMMITTEE CLEARANCE & PATIENTS OFFERING VOLUNTARY WRITTEN INFORMED CONSENT TO PARTICIPATE IN THIS STUDY
INCLUSION CRITERIA
1. Age >40 years
2. Patients diagnosed with Type 2 Diabetes Mellitus of 1 to 10 years duration.
EXCLUSION CRITERIA
1. Patients with CAD diagnosed by symptoms, ECG or regional wall motion abnormalities on echocardiogram or prior coronary angiography.
2. Patients with heart failure diagnosed by signs and symptoms, chest radiograph or echocardiography.
3. Patients with significant valvular heart disease, diagnosed clinically or with echocardiography.
4. Heart rate <50 or >100 beat per minute, atrial fibrillation and other
arrhythmias that may interfere with Doppler studies.
5. Hypertensive patients (Either a known case on treatment or when
blood pressure is greater than 140/90 mmHg) [7]
6. Patients with long history of diabetes mellitus (>10 years) or duration of < 1 year.
7. Subjects with poor transthoracic echocardiographic window.
STUDY PROTOCOL
This study will include all patients of Type 2 Diabetes Mellitus, greater than 40 years of age falling into criteria set by American
Diabetic Association. [8]
All patients will be subjected to the following investigations:
i. Hemogram
ii. Complete Urine Examination
iii. Diabetic Profile – FBS, PPBS. HbA1c
iv. Blood Urea, Serum Creatinine and Serum Electrolytes
v. Fasting Lipid Profile
DIAGNOSTIC CRITERIA FOR TYPE 2 DIABETES MELLITUS
Fasting blood sugar (FBS) ≥ 126 mg/dL
(or)
Post-prandial blood sugar ≥ 200 mg/dL
(or)
HbA1c ≥ 6.5% or Classic diabetes symptoms + random plasma glucose
≥ 200 mg/dL
DIAGNOSTIC CRITERIA USED IN 2D-ECHOCARDIOGRAPHY
Subjects will be examined using standard parasternal long axis, short axis and apical two and four chambers views. Conventional techniques (two-dimensional-2D, M-mode echocardiography, Pulsed-wave Doppler wave (PW) and TDI methods will be used for
1. LV internal dimensions: LV end systolic dimension (LVESD) and LV end diastolic dimension (LVEDD).
2. Ejection fraction (EF %) (Using Teichholz method).
3. E point (m/sec): Early diastolic velocities of mitral inflow (Doppler-derived).
4. Septal and lateral e point by tissue Doppler (m/sec): Early diastolic myocardial velocity, derived from tissue Doppler imaging.
5. E/e ratio: Ratio of early diastolic velocities of mitral inflow (PW-derived) and myocardial movement (TDI-derived) taken as left ventricular filling pressure.
6. Left atrial (LA) volume index (mL/BSA): In apical four and two-chamber views.
7. Peak tricuspid regurgitation (TR) velocity (m/sec). Systolic dysfunction was defined if LV Ejection fraction <50%.
DEFINITION OF LV DIASTOLIC DYSFUNCTION
Definition of LV diastolic dysfunction will be indicated if 3 or more of these variables are abnormal:
→ Septal e <7 cm/sec
→ Lateral e <10 cm/sec
→ E/e ratio >14
→ E/A ratio < 0.8
→ LA volume index >34 mL/m2
→ Peak TR velocity >2.8 m/sec.
Diastolic dysfunction will be divided into three grades :
• Grade I; impaired LV relaxation.
• Grade II ; pseudonormal filling pattern.
• Grade III ; restrictive filling pattern.
PARAMETERS USED FOR DATA ANALYSIS
The parameters used will be categorised separately for men and women.
→ Age
→ Duration
→ Body Mass Index (BMI)
→ Haemoglobin A1c (HbA1c)
→ E/A ratio
→ E/e ratio
→ Left Atrium Size (LA Volume Index)
→ Tricuspid Regurgitation Velocity (TR Velocity)
→ Left Ventricular Ejection Fraction (LVEF / EF)
→ Diastolic Dysfunction
* p value <0.05 is considered statistically significant and p value
<0.001 is considered highly significant.
LINK TO COMPLETE THESIS WITH MASTER CHARThttps://drive.google.com/file/d/1SGpYQm8U9aAnLMiNkz_Uv41PgIIC2vak/view?usp=sharing
LOG BOOK
AUGUST 09, 2021
LOG BOOK
MAY 2020
JUNE 2020
JULY 2020
AUGUST 2020
SEPTEMBER 2020
OCTOBER 2020
NOVEMBER 2020
DECEMBER 2020
CORE CLINICAL COMPETENCIES
AUGUST 09, 2021
Core clinical competencies:
A few selected procedural skills videos -
Ultrasound guided Lung Biopsy - 45 F - Lung biopsy in patient suspected with Bronchoalveolar carcinoma - by Dr. Aditya Samitinjay - YouTube
Ultrasound Guided Pericardiocentesis - 35yr M - Pericardial Tap by Dr. Aditya Samitinjay - YouTube
Ultrasound Guided Pericardiocentesis - Pericardiocentesis in a 56/F with severe anaemia with pericardial effusion by Dr.Aditya Samitinjay - YouTube
Clinical Discussions and Presentations - A few selected videos are shared in the playlist below -
Demonstration of Interesting Clinical Signs and a few learning points on Echocardiography
HALLTICKET NO. 18100006004
CASES.
LONG CASE:
AUGUST 09, 2021
CASE PRESENTATIONS
26 year old male, construction worker by occupation presented to the casualty with the chief complaints of
Fever since 3 months
Cough with expectoration since 2 months
Dyspnea on exertion since 2 months
Vomiting since 2 months
Decreased appetite and weight loss over last 2 months
Dark coloured stools since 2 weeks.
History of presenting illness:-
Patient was apparently asymptomatic 3months back till when he attended his relative function where he consumed alcohol for 2days (Around 8 beers) following which after 2days he developed high grade fever though not associated with chills & rigors or Night sweats and it subsided with medication for 1 week but from then he's having on & off fever.
The following month he started experiencing productive cough with mucoid expectoration, blood tinged amounting to 2 to 3 cup's per day it's foul smelling . Cough is more in sitting position & slightly relieved by Lying down on bed & It's more during day time than in night.
He also started feeling difficulty in breathing on walking for small distances . It's progressive & currently he has to take a break After walking for 100meters of distance.
He's having 2 to 3 episodes of vomiting daily containing food particles.
He also complains of loss of appetite and unintentional weight loss of around 10 kgs over the past 3 months from 72kgs to 62kgs.
History of black colour stools since 2weeks not associated with mucus or foul smelling.
No h/o chest pain, palpitations, syncopal attacks, profuse sweating, Orthopnea or paroxysmal nocturnal dyspnea
No h/o Headache, seizure, weakness of arms or legs
No h/o Regurgitation of food or epigastric burning pain.
Past history:-
Not a k/c/o Hypertension, Diabetes mellitus, Asthma, epilepsy, Tuberculosis or any heart diseases. No past history of allergies or surgeries.
Personal history:-
Diet- mixed
Appetite- decreased
Sleep-adequate
Bowel & bladder- normal
Occasional alcoholic, Occasional smoker.
Family history:-
No h/o similar complaints in family members
Drug history:-
Patient visited around 4 hospitals in past three month's where he's given multiple antibiotic injections, Antipyretics.. Etc
No h/o any drug allergies .
Summary at end of history:-
A 26yr old male who's a construction worker by occupation and who's an occasional smoker presented with persistent fever, cough with blood tinged expectoration and decreased appetite associated with weight loss since 2months and black color stools since past 2weeks and had a history of reccurent hospital visits & intake of medications for these complaints in past 2months with no history of Hypertension, diabetes or any contact with TB.
Differentaial diagnosis:-
Lung consolidation
Lung abscess
General physical examination:-
Patient conscious, coherent, cooperative
Moderately built & moderately nourished.
Height- 165cm
Weight- 55kgs
BMI- 20.2
Temperature - 100.6f
PR - 94bpm, Regular & normal volume, No radioradial or radio femoral delay.
All peripheral pulses felt
BP - 100/70mmhg Right arm supine position
RR - 28cpm, Abdominothoracic type.
Spo2 at 98 % on room air.
Pallor +nt
Icterus -nt
Cyanosis -nt
Clubbing -nt
Lymphadenopathy -nt
Edema -nt
No Nicotine staining over hand's, lips or any visible wasting of hand muscles
Spine appears normal
SYSTEMIC EXAMINATION:-
RESPIRATORY SYSTEM-
Patient examined in sitting position
Inspection:-
Upper respiratory tract - oral cavity, nose & oropharynx appears normal.
Chest appears Bilaterally symmetrical & elliptical in shape
Respiratory movements appear equal on both sides and it's Abdominothoracic type.
Trachea central in position & Nipples are in 4th Intercoastal space
No signs of volume loss
No dilated veins, scars, sinuses, visible pulsations.
Palpation:-
All inspiratory findings confirmed
Trachea central in position
Apical impulse in left 5th ICS, 1cm medial to mid clavicular line
Cricosternal distance is 3finger breadths.
MEASUREMENTS-
chest circumference- 31 inches at expiration & 32 inches at full inspiration
Chest expansion- 2.5cm
Right left
Hemithorax- 15.5 inches 15.5 inches
Hemithorax expansion- 1/2inch 1/2inch
AP diameter- 7 inch
Transverse diameter- 12 inches
AP/T ratio - 0.58
Respiratory movement's:- decreased on Right side.
https://drive.google.com/file/d/1t2cmYVK6yu6o3VcOhsvibeqqIxISZ8uS/view?usp=drivesdk
https://drive.google.com/file/d/1t41C_0FklIuSHq68BDEh0uEK43_srWWy/view?usp=drivesdk
Tactile vocal phremitus- increased in right Infraaxillary & infra scapular area.
Aegophony & whispering pectorloquy present in right Infraaxillary & infra scapular area
Percussion:-
Right left
Supraclavicular- Resonant (R) (R)
Infraclavicular- (R) (R)
Mammary- (R) Dull
Axillary- (R) (R)
Infra axillary- Dull (R)
Suprascapular- (R) (R)
Interscapular- (R) (R)
Infrascapular- Dull (R)
Auscultation:-
Right Left
Supraclavicular- Normal vesicular (NVBS)
Breath sounds (NVBS)
Infraclavicular- (NVBS) (NVBS)
Mammary- (NVBS) (NVBS)
Axillary- (NVBS) (NVBS)
Infra axillary- Tubular B.S (NVBS)
Suprascapular- (NVBS) (NVBS)
Interscapular- (NVBS) (NVBS)
Infrascapular- Tubular B. S (NVBS)
ABDOMEN :-
Inspection :
shape of abdomen appear normal & symmetrical
No Generalised/Localised distension seen.
All quadrants moving equally with respiration
Umblicus is central & inverted
Skin over the Abdomen- Looks normal
No visible Scars/Sinuses/Dilated/Prominent veins / peristalsis/Pulsations .
Palpation :
All Inspectory findings confirmed
Mild Tenderness in right hypochondrium
No Guarding/ Rigidity
Edge of liver is palpable on deep inspiration Spleen is not palpable
Percussion:-
Liver span is 15cm from right 4th ICS to right coastal margin along mid clavicular line
Spleenic dullness noticed in left coastal margin
Auscultation:-
Normal bowel sounds heard, no renal bruit heard.
CARDIOVASCULAR SYSTEM:-
Apical Impulse felt in left 5th ICS, no parasternal heave or precordial bulge felt
S1S2 heard
No murmurs heard.
CENTRAL NERVOUS SYSTEM:-
Higher mental functions intact
No FND, pupils-NSRL.
Cranial nerves- Intact
Motor & sensory systems- Normal.
PROVISIONAL DIAGNOSIS:-
Right lung lower lobe consolidation.
INVESTIGATIONS:-
Hemogram-
Hb- 9gm/dl
Tlc- 13,700cells/cu mm
Plt- 4lakh/cu mm
Rft:
urea- 10mg/dl
Creatinine- 0.9mg/dl
Sodium-129mEq/l
Potassium-4.1mEq/lChloride-94mEq/l
Lft:
Total bilirubin-2.28mg/dl
Direct bilirubin-0.52mg/dl
SGOT- 109 IU/L
SGPT-12IU/L
Alkaline phosphate- 313IU/L
Total proteins - 7.5gm/dl
Direct bilirubin-0.52mg/dl
SGOT- 109 IU/L
SGPT-12IU/L
Alkaline phosphate- 313IU/L
Total proteins - 7.5gm/dl
Albumin-2.7gm/dl
Esr- 90mm
PT-INR - 20 sec & 1.1
APTT- 39sec
BT & CT - 2min & 5min
HIV, HBSAG, HCV- Negative
ECG:-
USG chest:- Consolidatory changes noted in right lower lobe.
Chest xray-
USG abdomen- A large hypoechoeic lesion measuring 8cm × 8cm in right lobe of liver.
CECT abdomen-
Final diagnosis:- Amoebic liver abscess with rupturing into pleural cavity with Right lung basal consolidation.
Initially conservative management is planned
Treatment:-
1.Inj. Metronidazole 750mg/iv/Tid
2.inj.Ceftriaxone 1gm/iv/bd
3.Inj.pantoprazole 40mg/iv/OD
4.inj paracetamol 1gm/Iv/sos
5.Tab.paromomycin 500mg/Tid
6.syp.Ambrolyte 5ml/Tid
7.Temperature/Respiratory rate /blood pressure/SpO2monitoring.
Treatment & vitals charting:-
Discussion:-
Amoebic liver abscesses most commonly noticed in the age group of 20–45 years and have been noted infrequently in the extremes of ages, with an adult male to female ratio of 10:1 . Our case is of a 26-year-old male patient who presented with the complaint of fever, Cough with Expectoration that's blood tinged, SOB, weight loss for the past three months.
The diagnosis of amoebic liver abscess is sometimes difficult since its clinical manifestations are highly variable, like in our patient who presented with a long standing cough with blood tinged expectoration, intermittent high-grade fever, and progressive dyspnoea & weight loss in spite of not having symptoms like right upper quadrant abdominal pain, jaundice,, the patient still had the disease.
We report a case of Right lung lower lobe consolidation with central liquefaction secondary to an Ruptured amoebic liver abscess that was misdiagnosed as pneumonia & he was been on multiple antibiotics in outside hospitals. Pleuro-pulmonary amoebiasis is easily confused with other illnesses, and it is treated as pulmonary TB, bacterial lung abscess, and carcinoma of the lung.
Aspiration and drainage of pus from thoracic empyema usually will be helpful but in our case it's not presented as empyema
Also, it has been recommended that amoebic liver abscess be treated with metronidazole or tinidazole plus a luminal amoebicide (eg. paromomycin or iodoquinol) even if the intestinal infection is not documented.
Imaging techniques such as ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) have excellent sensitivity for the detection of a liver abscess and were used with our patient, but these techniques cannot distinguish amoebic abscesses from pyogenic abscesses or necrotic tumor. The diagnosis of an amoebic liver abscess is confirmed with either serologic or antigenic testing. It can also be coupled with stool microscopy and antigen testing of the stool, with or without evaluation for the parasite in the hepatic abscess fluid.
Due the combination of findings in the imaging studies like hepatomegaly, pleural effusion with thick loculated collection, obliteration of costophrenic angles, left subdiaphragmatic collection, and involvement of the right lung which suggested an basal consolidation of the right lung, the patient was treated with a percutaneous liver abscess drainage. Following drainage, the fever improved dramatically as he continued to be under observation.
Some literature indicates that percutaneous needle aspiration or catheter drainage may be helpful for large abscesses (over 5-10 cm), in particular, if the diagnosis is uncertain, if there is an initial lack of response, or if a patient is very ill, suggesting impending abscess rupture, while some authors have had higher thresholds of maximum diameter >10.5 cm and intervention only in the absence of response to drugs . Henceforth, for those cases that fail to respond to the conventional management, interventions such as needle aspiration, catheter drainage, or surgical interventions can be employed as required.
Link's to similar case report's
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SHORT CASE- 1:
A 44 year old male patient, farmer by occupation came to OPD with chief complaints of Pedal edema since 3 months
Shortness of breath since 2months
HISTORY OF PRESENT ILLNESS
The patient was apparently asymptomatic 3months back then he developed bilateral pedal edema pitting type, initially it's below ankle & subsided in early morning's, later it's gradually progressed to below the knee and not assocaited with diurnal variation.
He then developed shortness of breath since 2months, insidious in onset & gradually progressed from grade 1 to grade 2 to 3 currently.
He's also having peri orbital edema & facial puffiness predominantly in morning since 2mnths
He has decreased urine output since 2mnths
No h/o hematuria, fever, chest pain, palpitations, diaphoresis, syncopal attacks
HISTORY OF PAST ILLNESS:-
He has tested positive for covid-19, 3 months back & recovered after using medication.
known case of Hypertension since 1 year [on tab CILACAR 10mg - morning, 20mg - night].
Not known case of DM, Asthma, TB, Epilepsy, CAD
PERSONAL HISTORY
He is married
Occupation - farmer
Diet - Mixed
Appetite - Normal
Bowels - Regular
Micturition - decreased urine output
He has no known allergies
Occasional Alcoholic since 20 years and stopped 3 months back.
No smoking
FAMILY HISTORY
No significant family history
DRUG HISTORY
He has been using Tab. CILINDIPINE 10mg - morning, 20mg -night for Hypertension since 1 year.
SUMMARY AT THE END OF HISTORY:-
A 44yr male patient farmer by occupation who's an occasional alcoholic presented with c/o pedal edema, Sob & decreased urine output with a past history of hypertension and Not a k/c/o DM/Asthma/CAD.
Differential diagnosis:-
Chronic kidney disease
GENERAL EXAMINATION
Patient is conscious, coherent, cooperative and examined in well Lightned room.
VITALS
Pulse rate -94bpm
Respiratory rate - 28cpm/min
BP - 140/90mmHg
Temperature - Afebrile
SpO2 - 98% at room air
GRBS - 141mg%
PHYSICAL EXAMINATION
Pallor - present
Icterus - absent
Cyanosis - absent
Clubbing of fingers/toes - absent
Lymphadenopathy - absent
Edema of feet- present, pitting type
SYSTEMIC EXAMINATION
CARDIOVASCULAR SYSTEM
Jvp elevated
Apex beat in left 5th ICS 1cm lateral to mid clavicular line
S1 and S2 heard
No thrills/parasternal heave / murmurs heard
RESPIRATORY SYSTEM
.Vesicular breath sounds heard in all area's
.No wheezing
.No adventitious sounds heard
ABDOMEN:-.No tenderness
.No palpable mass
.No free fluid
.No Audible bruits
.Liver and spleen are not palpable
.Bowels sounds are heard 
SERUM CREATININE 
PROVISIONAL DIAGNOSIS
CNS
Conscious,normal speech
No signs of meningeal irritation
Normal gait
Cranial nerves are intact
Motor system normal
Sensory system normal
Reflexes normal
DIAGNOSIS:-Chronic kidney disease secondary to hypertension.
INVESTIGATIONS
INVESTIGATIONS
29/7/2021
ULTRASOUND 
BLOOD UREA 
SERUM ALBUMIN
ECG
HEMOGRAM
COMPLETE URINE EXAMINATION
TOTAL SERUM PROTEINS (A/G RATIO)
4/8/2021
SERUM ELECTROLYTES
SERUM IRON
PROVISIONAL DIAGNOSISChronic Renal Failure
TREATMENT
T.Lasix 40 mg PO/BD
T.Cilacar 10 mg PO/OD
T.Nodosis 500mg PO/OD
T.orofer XT PO/BD
T.Cilacar 20 mg PO/OD
Inj.Erythropoietin 4000IU (weekly twice)
Fluid Restriction <1.5L/day
Salt restriction <4gms /day
--------------------------------------------------------------------------------------------
SHORT CASE- 2:
A 35yr old female patient who's a bank employee by occupation came to casuality with chief complaints of involuntary movements of right upperlimb & lowerlimb since afternoon 2pm.
History of presenting illness:-
Patient was apparently asymptomatic till today morning, when she developed mild weakness of her right upperlimb & lowerlimb for which she went to local hospital & got few medications & later it subsided, she then attended her bank work where at around 2pm she had sudden involuntary movements of right upperlimb & right lowerlimb which lasted for 2 to 3 minute's, She had around 5 similar episodes with a time gap of 10minutes.
They're associated with post ictal drowsiness & are not associated involuntary micturition/defaecation/uprolling of eyeballs/ Tongue bite/deviation of mouth/automatic behavior like running, walking about, Violent behavior.. Etc.
She had an similar episode in casuality & she's having post ictal confusion & drowsiness.
From the next day she's drowsy & complained of headache & vomitings.
No h/O palpitations/syncopal attacks/facial deviation/dysphagia/chest pain/ orthopnoea /PND/Neck pain/Projectile vomiting/
Past history:-
No h/O similar complaints in past
Not a k/c/o Hypertension/Diabetes mellitus/ Asthma/epilepsy/TB/CAD/Migraine/Thyroid disorders/psychiatric disorders.
Drug history:-
No known drug allergies/No history of any chronic medications/Oral contraceptive pills intake.
Family history:-
No h/O similar complaints in family members.
Personal history:-
Sleep- Adequate
Appetite- normal
Bowel & bladder - regular
No addictions.
Summary at the end of history:-
A 35yr old female who's a bank employee came with complaints of repeated episodes of involuntary movements of right upperlimb & right lowerlimb since afternoon which are associated with post ictal confusion & drowsiness & later she had headache & vomitings.
Differential Diagnosis:-
Complex partial seizures secondary to Cerebrovascular accident/ cerebral venous thrombosis.
General examination :-
Pt is drowsy
No pallor/icterus/cyanosis/ clubbing Lymphadenopathy/ edema/
Temperature - Afebrile
Pulse rate -90 beats per minute ,regular, normal volume ,vessel wall normal ,no radio-radial or radio femoral delay, All peripheral pulses felt.
Bp- 110/70mmhg in both arm's supine position
Respiratory rate- 20cpm
Grbs - 109mgdl
SYSTEMIC EXAMINATION:-
Central nervous system-
Patient is drowsy.
GCS - E3V3M3
Pupils- Normal size & reactive to light.
Cranial nerves- corneal reflex +nt
No fixed gaze seen, patient is able to look at all sides on repeated verbal commands.
Vestibulooccular reflex intact.
Motor system:-
BULK- Appears normal on both sides
TONE - Right Left
Upper limb- Normal Normal
Lower limb- Normal Normal
POWER - couldn't be tested. But the patient is moving all her limbs on bed.
Right Left
Reflexes-
Biceps. +
Triceps. + +
Supinator. + +
Knee. - -
Ankle. - -
Superficial reflexes
Corneal. + +
Conjunctival. + +
Plantars. Extensor. Extensor
Sensory system:-
Moving her body to Deep pain & crude touch in all areas of body.
Anterior Spino thalamic Tract:-
Crude touch: + +
Lateral Spino thalamic Tract:-
Pain. + +
Temperature. Cannot be examined
Posterior column : cannot be examined
Fine touch. -
Vibration. -
Joint position. -
Rombergs. -
Cortical: Cannot be elicited
Two point discrimination -
Tactile localization. -
Stereognosis. -
Graphesthesia. -
Gait: cannot be examined
Sign's of meningeal irritation:-
No neck stiffness.
Brudzinski sign absent
No kernigs sign
Cardiovascular system:-
Apical Impulse felt in left 5th ICS,
No visible pulsations in neck
No parasternal heave or precordial bulge felt
Both heart sounds S1S2 heard
No murmers heard.
Respiratory system:-
Bilateral air entry present
NVBS, No added sounds heard.
Provisional diagnosis:-
Acute complex partial seizures of Tonic clonic variety involving Right upperlimb & Right lowerlimb secondary to CVA/CVT.
Investigations:-
Hemogram-
Hb- 12gm/dl
Tlc- 4,700cells/cu mm
Plt- 3.4lakh/cu mm
Rft:
urea- 10mg/dl
Creatinine- 0.9mg/dl
Sodium-139mEq/l
Potassium-4.1mEq/l
Chloride-99mEq/l
Lft:
Total bilirubin-1.28mg/dl
Direct bilirubin-0.52mg/dl
SGOT- 69 IU/L
SGPT-12IU/L
Alkaline phosphate- 113IU/L
Total proteins - 7.5gm/dl
Albumin-3.7gm/dl
Esr- 18mm
CUE- No pus cells/rbc/proteinuria
Fundoscopy:- Normal.
TREATMENT:-
1.Inj Levetericetam 1gm/Iv/Stat followed by
Inj.Levetericetam 500mg/Iv/Bd
2.Inj pantoprazole 40mg/iv/od
3.Inj.mannitol/100ml/Bd
4.Ryles tube insertion & feeding.
5.Temp/pr/Bp/SpO2 monitoring
6.Inform SOS, if seizure reccurs.
Here's the Link to video of her seizures.
HALL TICKET NO. 18100006004
THESIS
AUGUST 09,2021
TITLE:
ACID BASE CHANGES IN ACUTE DIARRHEAL DISEASES IN A RURAL TERTIARY CARE HOSPITAL
INTRODUCTION:
Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. Disorders of acid-base homeostasis complicate a variety of disease conditions and contribute to morbidity and mortality. If not promptly recognized, these disorders interrupt normal functioning of various organ systems and ultimately prove fatal. The clinical settings in which such acid-base disorders occur are numerous, an attempt to list out all the causes of acid-base disturbances will be exhaustive and unwarranted. Nevertheless, to make some simplification, it can be said, diseases of the lungs and kidneys (the two important organs involved in acid-base homeostasis), contribute to an important proportion of such acid base disturbances.
Acute Diarrheal Disease is yet another cause of acid-base and electrolyte disturbance and the present study aims to explore the various changes that take place in the acid base status of patients who suffer an acute diarrheal disease. Diarrhea can cause a variety of fluid volume, acid-base, and electrolyte abnormalities and causes alterations in serum chemistries. The study tries to validate a prognostic role for those acid-base changes in acute diarrheal disease and calls for an early recognition and correction of acid-base changes.
AIM:
To Study Acid base changes in patients with acute diarrhea.
OBJECTIVES:
1. To Determine the acid-base disturbances (ABG, ANION GAP) resulting from acute diarrheal disease.
2. To study the changes in acid-base status in patients with acute renal failure due to acute diarrheal disease.
3. To find out severe metabolic acidosis (pH < 7.2 or pH=7.2) in acute diarrheal disease.
4. To study the outcome of patients in relation to severity of metabolic acidosis.
MATERIALS AND METHODS
Study Design
This study is a prospective study
Study Setting
All patients with acute diarrhea admitted in Department of General Medicine, Kamineni
Institute of Medical Sciences, Narketpally, Nalgonda (Dist),Telangana .
Study Period
This study was conducted between October 2018 to September 2020.
Inclusion Criteria
Patients More than 12 years of age, who presented with acute diarrheal were included.
Both sexes are included in the study.
Exclusion Criteria
Since this study aims at identifying the acid-base changes occurring as
a result of acute diarrhea, the following patients were excluded.
1) Patients who had coexisting diseases like chronic obstructive pulmonary disease(COPD),
Patients with Diabetes Mellitus (who might have Type IV RTA –
hyporeninemic hypoaldosteronism), Hepatic disease and chronic kidney diseases are excluded, because these Diseases might themselves produce Changes in ABG.
2) Patients who are taking drugs that are likely to produce Acid-Base disturbances are also excluded.
Ex. Metformin (for PCOD)
Cholestyramine
Calcium or Magnesium chloride
Acetazolamide
3) Drugs causing RTA (Renal Tubular Acidosis)
Ex. Cotrimoxazole
Spironolactone
Triamterene
STUDY POPULATION
The study included 72 patients, 40 males and 32 females. The youngest patient in the study was 13 years of age and the oldest patient was 85 years of age. All satisfied the inclusion and exclusion criteria.
STUDY PROTOCOL AND LABORATORY INVESTIGATIONS
In all patients preliminary history regarding duration of Loose Stools, presence of vomiting and Reduced Urine output was recorded. Clinical examination was done to identify the degree of dehydration, acidotic breathing if any, vital signs and other systems examination to rule out
any preexisting diseases that might confound the acid-base picture. In all patients routine urinalysis for albumin, sugar deposits were done. Also urine was examined for acetone, since patients with diarrhea might starve leading to starvation keto acidosis. In all patients hemogram was routinely done. It is mandatory to know the hemoglobin level for determining oxygen content of blood in ABG analysis. If any of the patients were found to have renal failure (defined as serum creatinine > 2mg %), subsequent serial measurements were made as appropriate and after treatment.
Treatment Protocol Followed
All patients were treated for rehydration with oral fluids, ORS and with IV Fluids (2:1 saline, lactate cycle) as required. (34) If any patient was found to have severe acidosis (PH< 7.2) bicarbonate was administered intravenously. About 50-75ml. of 7.5% sodium bicarbonate was slowly infused intravenously over a period of one hour. If the patient presented with raised renal parameters fluid challenge with 1.0 to 1.5 liters of IVF was given. If the patient shows any improvement in urine output and clinical Signs and Symptoms, rehydration therapy was continued. If the patient had persistent oliguria despite rehydration and other uremic manifestations mandating dialysis, peritoneal or haemodialysis was undertaken.
Regular monitoring of renal functions was also done. Antibiotics were given as appropriate. Patients were discharged once diarrhea stopped and renal functions returned to normal if they initially had renal failure.
MASTER CHART:
LINK TO COMPLETE THESIS WITH MASTER CHART:
18100006004 PROCEDURAL COMPETENCIES
AUGUST 09, 2021
PROCEDURAL COMPETENCIES:
1.LUMBAR PUNCTURE:
2.FEMORAL VEIN CATHERIZATION:
HALL TICKET NO. 181000060005
CASE PRESENTATIONS
AUGUST 09, 2021
LONG CASE:
History taken from patient's wife and younger son and is reliable . A 59yr old male patient who is a right handed, resident of Hayathnagar, carpenter by occupation presented with chief complaints of
-decreased appetite since 6 months
-yellowish discolouration of eyes and urine since 6months
-difficulty in passing stools since 3months
-altered behaviour since 1month
History of present illness :
Patient was apparently alright 6months back. Then he had fever -low grade Intermittent, not associated with chills and rigors, lasting for 45days, relieved on taking medication. Associated with decreased appetite.
Complaints of yellowish discolouration of eyes and urine for which he consumed Ayurvedic medicine powder.
In April 2021 he consumed leaf medicine for prevention of corona, after that he had difficulty in passing stools (passed stools every 4-5days), not relieved by taking laxatives and enema.
Then he developed abdominal distention-acute in onset, diffuse, gradually progressive associated with pedal edema and scrotal swelling, relieved on paracentesis (2-2.5litres) and albumin infusion.
Not associated with facial puffiness. Associated with vomiting-greenish, 4-5episodes, non projectile, contained bile and food particles what ever he consumed.
Complaints of altered behaviour, staring look, not responding to speech, irritable since 1 month and got hospitalized, improved on medication and got discharged.
Since 6 days patient became drowsy, excessive sleeping, and constipation and loss of appetite. Complaints of rash over upper thorax since 6days.
No h/o pain abdomen
No h/o Melena.
No h/o hematemesis.
No h/o breathlessness, chest pain
No h/o dysphagia
No h/o weight loss
No h/o decreased urine output
Past history:
History of jaundice every 6-8months since 20yrs
History of surgery for sinusitis 7yrs back
History of RTA (fall from byke) and injury to left thigh 3yrs back
Not a known case of hypertension, diabetes, epilepsy, asthma, Tuberculosis, thyroid disorder, CAD.
Family history:
No similar complaints in family
Personal History:
Marital status: Married
-Mixed diet
-Loss of appetite
Alcoholic -since 40yrs (consumed 2beers (24gm of alcohol) daily
No habit of smoking or tobacco chewing
Bladder habits regular and normal
Bowels -constipation since 4months
Sleep -excessive day time sleepiness.
Socio economic status: upper middle class
Drug history :
Took ayurvedic leafs 4months back
And consumed Ayurvedic powder every time he had jaundice.
No h/o any drug allergy
Summary: A 59 year old male, carpenter by occupation, who is a chronic alcoholic and non hypertensive and non-Diabetic presented with decreased appetite and yellowish discolouration of eyes and urine since 6months, difficulty in passing stools since 3months and altered behaviour since 1month and became drowsy since 6days with history of ascites 1month back.
Provisional diagnosis:
1. Decompensated chronic liver disease with cirrhosis secondary to alcohol -stage 3 hepatic encephalopathy.
Differential Diagnosis:
1. Chronic liver disease secondary to alcoholism
2.acute liver injury secondary to leaf medicine
3.cirrhosis secondary to NAFLD
4.Cirrhosis secondary to hepatitis
General examination:
Moderately built and nourished
Patient is drowsy, arousable, not cooperative and not responding to commands.
GCS: E3V1M5
BMI: 24.8kg/m²
Vitals:
Pulse - 95beats per minute, regular, normal volume, vessel wall normal, no radio-radial delay, no radio femoral delay, all peripheral pulses felt.
Blood pressure:
right arm -110/80mmHg, supine position
Left arm -110/80mmHg, supine position
Right leg - 130/80mmHg
Left leg -130/80mmHg
Respiratory rate- 18cycles per minute, abdominothoracic, no usage of accessory muscles.
Temperature - 98.2F
SpO2-98% at room air
JVP - not elevated
Physical examination:
Pallor +
Icterus+
No cyanosis
No clubbing
No generalized lymphadenopathy
Pedal edema +
B/l Parotid enlargement +
No alopecia
No fetor hepaticus
No gynecomastia
No asterexis
Axillary hair sparse
Spider never +
No Palmar erythema
Flanks full
Dilated veins over abdomen
No testicular atrophy
No loss of pubic hair
Systemic examination:
Gastrointestinal system
Inspection:
Oral cavity - no dental caries, no tobacco staining.
Abdomen- Flanks full, mild distenstion+
Skin over abdomen normal
Umbilical-normal in position
Movement of corresponding quadrants normal with respiration
Dilated veins +
No visible peristalsis, no visible pulsation,
No scars or sinuses.
Hernias orifices -normal
Palpation:
No local rise of temperature
Abdomen soft
No guarding and rigidity
All inspection findings confirmed
Lower border of liver not palpable
Spleen not palpable
Kidneys- bimanually palpable, ballotable
Fluid thrill absent
Abdominal girth -92cms
Spino umbilical distance -
. right- 46cm left-46cm
Xiphisternum to umbilucus -16cms
Pubic symphisis to umbilicus-11cms
Per rectal examination- no mass felt, no blood staining, hard pellets+
Hernias orifices -normal
Percussion:
Shifting dullness +
Liver span - 11cm
Traubes space - resonance
Auscultation:
Bowel sounds +( 6 per minute)
No hepatic bruit, no venous hum
Examination of scrotum: No testicular atrophy
Examination of spine - normal
CENTRAL NERVOUS SYSTEM:
Higher mental functions:
Patient is drowsy, non cooperative
Not oriented to time, place, person
Speech - aphasia
MMSE - Cannot be done
Kirby's method:
General reaction and posture:
Patient is drowsy, apathetic
Patient is not responding and moving when placed in awkward position.
Eyes and pupils :
Eyes open with decreased blinking
Reaction to examiners questions and tests:
Not responding to commands
Cranial nerves - intact
Motor examination:
Attitude - lying over bed with knees flexed
Bulk -no apparent wasting present
Tone - right. Left
UL. Hypo. Hypo
LL. Hypo. Hypo
Power-
UL. 3/5. 3/5
LL. 3/5. 3/5
Reflexes-
Biceps. ++ ++
Triceps. ++ ++
Supinator. + +
Knee. - -
Ankle. - -
Superficial reflexes
Corneal. + +
Conjunctival. + +
Plantars. Flexion. Flexion
Abdominal. +
Cremastric. +
Perianal. +
Sensory examination:
Spino thalamic:
Crude touch: + +
Pain. + +
Temperature. Cannot be examined
Posterior column: cannot be examined
Fine touch. -
Vibration. -
Joint position. -
Rombergs. -
Cortical: Cannot be elicited
Two point discrimination -
Tactile localization. -
Stereognosis. -
Graphesthesia. -
Gait: cannot be examined
Spine: No bony tenderness no kyphosis, scoliosis
Cranium - no bony deformities
Peripheral nerves- no thickened nerves, no foot drop, no wrist drop
Other systems:
CARDIOVASCULAR SYSTEM:
S1S2 heard
No murmurs
Apex -normal
Respiratory system:
Inspection:-
Upper respiratory tract - oral cavity, nose & oropharynx appears normal.
Rules tube in place .
Chest appears Bilaterally symmetrical & elliptical in shape
Respiratory movements decreased on right Infra Mammary and right infrascapupar region.
Trachea central in position
Nipples are in 4th Intercoastal space
No signs of volume loss
No dilated veins, scars, sinuses, visible pulsations.
Palpation:-
All inspection findings confirmed
No local rise of temperature.
Trachea central in position
Apical impulse in left 5th ICS, 1cm medial to mid clavicular line.
MEASUREMENTS-
chest circumference-
82cms at expiration
85.5 cms at inspiration
Chest expansion- 3.5cm
Right left
Hemithorax- 41cms 41cms
Hemithorax expansion- 1.5cms 2cms
AP diameter- 20 cms
Transverse diameter- 35cms
AP/Transverse ratio - 0.57
Percussion:-
Right left
Supraclavicular- Resonant resonant
Infraclavicular- Resonant. Resonant
Mammary- Resonant Resonant
Inframammary. Stony Dull. Resonant
Axillary- Resonant Resonant
Infra axillary- stony dull Resonant
Suprascapular- Resonant Resonant
Interscapular- Resonant Resonant
Infrascapular- stony Dull Resonant
Auscultation:-
Right Left
Supraclavicular- NVBS. NVBS
Infraclavicular- NVBS NVBS
Mammary- NVBS NVBS
Infra Mammary- decreased NVBS
Axillary- NVBS NVBS
Infra axillary- Decreased. NVBS
Suprascapular- NVBS NVBS
Interscapular- NVBS NVBS
Infrascapular- decreased NVBS
Provisional Diagnosis :
1.Decompensated chronic liver disease with cirrhosis secondary to alcohol with stage 3 hepatic encephalopathy without portal hypertension and with moderate ascites and no signs of spontaneous bacterial peritonitis.
2. Anemia of chronic disease
3. right sided pleural effusion secondary to hydrothorax or hypoalbumunemia.
Based on history and examination we advised following investigations
Hemogram:
Hemoglobin-9.9 gm/dl
Total counts - 8500 cells/cumm
Neutrophils-74%
Lymphocyte-10%
Platelets- 1.79 lakhs/cumm
Peripheral smear - NC/NC Anemia
Complete urine examination:
Colour -pale yellow
Albumin nil
Pus cells nil
RBC - nil
Renal function tests:
Urea - 73mg/dl
Creatinine - 1.2mg/dl
Uric acid - 8mg/dl
Calcium - 10mg/dl
Phosphorus- 7mg/dl
Sodium - 128 mEq/l
Potassium - 3.8mEq/l
Chloride- 92mEq/l
LFT:
Total bilirubin -1.82
Direct bilirubin- 0.48
AST- 20
ALT- 10
ALP- 207
Total proteins -6.1
Albumin -2.2
A/G ratio - 0.51
PT -16 seconds
INR-1.11
aPTT- 32 seconds
Blood group - O positive
ÀBG:
PH: 7.44
PCO2 :34.2 mmHg
PO2: 89mmHg
HCO3: 24.2mmol/L
BEB: -0.2mmol/L
O2 sat: 96. %
USG abdomen: mild ascites
ECG
Chest x-ray:
MRI BRAIN - NORMAL
Discussion
What is hepatic encephalopathy?
Hepatic encephalopathy is the term used to describe the complex and variable changes in neuropsychiatric status which complicate liver disease. This syndrome is the defining feature of fulminant hepatic failure and, in this setting, is only one of a multitude of metabolic abnormalities caused by loss of functioning hepatocyte mass.
Precipitating factors:
1. Infections
2. Gastrointestinal Bleeds (GI Bleeds)
3. Dyselectrolytemia –Hyponatremia and Hypokalaemia
4. Dehydration – Fluid Restriction, Diarrhea/Vomiting, Excessive Diuresis
And Paracentesis
5. Constipation
6. High Protein Diet
Guideline Based Management of Hepatic Encephalopathy
1. Primary Intervention –
Correct or Eliminate the Precipitating Factor.
2. Dietary Advice
a. Dietary restriction of Protein is NOT RECOMMENDED. Conclusively demonstrated that limiting protein-calorie intake is not of benefit in patients with HE.
The recommended daily dietary allowance is 60-80g.
b.Vegetable and Dairy protein is recommended over animal protein because of a favourable calorie-to-nitrogen ratio.
3. BCAA (Branched Chain Amino Acids) supplementation has modest efficacy and it’s routine use is not recommended.
Medical Management
1. Non-Absorbable Disaccharides
Lactulose , Lactitol - First line agents; Symptomatic improvement only, no improvement in Psychometric test performance
Goal of Therapy – 2 to 3 Soft Stools per day.
2. Oral Antibiotics – Rifaximin 550 mg BD. Other Drugs – Neomycin, Metronidazole and Vancomycin.
3. Acarbose – An Intestinal α-Glucosidase Inhibitor
•Used in patients with cirrhosis and adult-onset Diabetes Mellitus
• Good fasting and post-prandial glucose control
•Lowered HbA1c (and post-prandial C-peptide levels)
• No alteration in biochemical parameters of Liver function.
4. Other Drugs (requiring conclusive evidence for use in clinical practise)
•Sodium benzoate, Sodium Phenylbutyrate and Sodium Phenylacetate (Urea cycle defects), Zinc supplementation,
•Extracorporeal Albumin Dialysis using MARS (Molecular Adsorbent Recirculating System)
5. L-Ornithine-L-Aspartate (LOLA)
•Significant decrease in Ammonia
Levels (Independent Predictor of
Survival)
• Improvement in Mental Status
• Better performance in
Psychometric tests
• Improved EEG Activity
Rifaximin vs placebo treatment in hepatic encephalopathy:
Polyethylene glycol vs lactulose in hepatic encephalopathy:
-------------------------------------------------------------------------------------------------
SHORT CASE- 1:
History given by patient and her husband and is reliable
A 45year old female, right handed, housewife, resident of Nalgonda presented with
chief complaints of
-headache since 2years
-Bilateral Knee,ankle,elbow joint pains since 6months
-weakness of right upper and lower limbs since 30days
-deviation of mouth to left since 30days
-Double vision since 10days
History of present illness:
Patient was apparently alright 2years back, then she developed headache-acute in onset, Intermittent, throbbing type, diffuse and bilateral. Not associated with nausea vomitings, photophobia, phonophobia, laceration, blurring of vision.
Complaints of bilateral Knee, ankle, elbow joint pains since 6months -not associated with fever, restriction of movements, early morning stiffness, swelling of joints -relieved by taking analgesics and aggrevated on exertion.
Complaints of weakness of right upper and lower limb since 1month -acute in onset and gradually progressive - initially she had mild symptoms, that gradually progressed over 1 month to current status. Initially she used to walk alone till the bathroom with some difficulty, later patient found difficulty in walking without support and patient felt more giddiness while walking.
Complaints of mild deviation of mouth to left side, not associated with drooling of saliva
Complaints of Double vision since 1month- intermittent, horizontal and binocular, no history of black spots, colored halos, floaters, blurring of vision.
No history of tingling and numbness
No history of difficulty in perceiving hot and cold sensation while bathing.
No history of perceiving band link sensation/girdle like sensation.
No history of electric shock like sensation.
No history of sensation of walking on cotton wool.
No history of washbasin attacks.
No history of loss of consciousness.
No history of memory loss.
No history of delusions, hallucinations, behavioral disturbances.
No history of alteration in smell.
No history of blurring of vision /able to differentiate colors.
No history of drooping of eyelids.
No history of loss of sensation over face.
No history of difficulty in closing eyes, lips
Able to perceive taste sensation.
No history of hard of hearing, ringing sensation in ears.
No history of regurgitation of food and fluids.
No history of difficulty in swallowing foods/nasal twang in speech.
No history of difficulty in moving neck in all directions, shrugging the shoulders.
No history of difficulty in pushing the food backwards, able to roll the tongue and clear the food.
No history of giddiness after getting up from bed.
No history of excessive sweating.
No history of Bowel and Bladder disturbances.
No history of recurrent infections.
No history of ear discharge, fever, neck stiffness, weight loss.
No history of drug intake.
No history of trauma and head injury.
Past history:
Non Diabetic, Non Hypertensive, No history of Asthma, CAD, Epilepsy.
She underwent hysterectomy 20 years back.
Family history :
She was married at the age of 18 years, 3rd degree consanguinity
1 st child- spontaneous vaginal delivery - 25 yrs old
2 nd child-vaginal delivery, died at 1 month of age due to unknown reason
3rd child - died at the age of 21 due to kidney failure
No history of similar complaints in family.
Personal history:
Mixed diet
Sleep adequate
Bowel and Bladder habits regular
No addictions
Socio economic status - lower middle class
Menstrual history:
Age of menarche: 15 years, regular cycles-5/30, no dysmenorrhoea
Drug history:
Patient was on
T.ECOSPIRIN 75mg/PO/OD
T.ATORVAS 20mg/PO/HS
Summary:A 45 year old right handed female patient, who is non hypertensive and non Diabetic with no addictions presented with headache since 2years and progressive weakness of right upper and lower limb since 1month and double vision double since 10days.
Differential Diagnosis:
1.Cerebro vascular accident involving mid brain and Pons
2. Basilar artery occlusion
3.Demyelinating disorders
General examination:
Pt conscious, coherent, cooperative
oriented to time, place and person.
Moderately built and nourished.
BMI: 24.6kg/m²
Vitals:
Pulse: 82beats per minute, regular, normal volume, vessel wall normal, no radio-radial delay, no radio femoral delay, all peripheral pulses felt.
Blood pressure:
right arm -120/80mmHg, supine position
Left arm -120/80mmHg, supine position
Right leg - 130/80mmHg
Left leg -130/80mmHg
Respiratory rate- 16cycles per minute, thoracoabdominal, no usage of accessory muscles.
Temperature - 98.2F
SpO2-98% at room air
JVP - not elevated
Physical examination:
No Pallor, icterus, cyanosis, clubbing, generalized lymphadenopathy, edema.
Systemic examination:
Patient is conscious, coherent and cooperative
Right handed person
MMSE - 30/30
Nystagmus -absent
Speech - spontaneous with intact naming ,repetition,fluency.
Spine -normal
Cranium -normal
gait -hemiplegic gait
Cranial nerves - right. Left
1.Sense of smell normal. Normal
2.Visual acuity - normal. Normal
Field of vision- normal. Normal
colour vision. Normal. Normal
fundus. Normal. Normal
3,4,6: extra ocular movements:
-restriction in adduction elevation, depression on right side and normal on left side
-pupils: Normal size and reacting to light on both sides
-direct and consensual light reflexes normal in both eyes
No Nystagmus
no ptosis
5. Sensory: sensations over face normal on both sides
Motor - massager, temporarily, pterygoids normal
7.motor: loss of nasolabial fold on right. Orbicularis ocular, orbicularis Oris, occipital frontalis, buccinator -normal on both sides
Sensory: taste over anterior 2/3rd of tongue normal on both sides
8.Rinnes test normal on both sides
. Webers test normal on both sides
9.10.uvula, palatal arch movements normal.
Gag reflex. - normal
Palatial reflex - normal
11.tarpezium and sternocleidomastoid -normal
12. No wasting and fasciculations
Tongue protrusion to midline.
Motor system examination:
1.Bulk (nutrition): right. Left
Inspection. Normal. Normal
Measurements: U/L 26/22cm 26/22cm
L/L. 46/ 34cm. 46/34cm
2.Tone: U/L hypotonia. Normal
L/L. Hyportonia. Normal
3.power:
Neck muscles. 5/5. 5/5
Upper limb:
Shoulder- -4/5. 5/5
Elbow - -4/5. 5/5
Wrist - -4/5. 5/5
Handgrip- 50% 100%
Lower limb:
Hip - 3/5. 5/5
Knee- 3/5. 5/5
Ankle - 3/5. 5/5
Trunk muscles- normal.
Deep tendon Reflexes - right left
Biceps +++ +++
Triceps +++ +++
Supinator ++ ++
Knee. +++ +++
Ankle. +++ +++
Jaw jerk. Present
Superficial reflexes -
Corneal. + +
Conjunctival. + +
Pharyngeal. + +
Palatal. + +
Abdominal. + +
Cremastric. + +
Plantar. Extensor extensor
Sensory system examination:
Spinothalamic: right. Left
Crude touch - normal. Normal
Pain- normal. Normal
Temperature- normal. Normal
Posterior column
Vibration sense- normal Normal
Fine touch - normal. Normal
Position sense - normal. Normal
Cortical senses
2point descrimination- normal. Normal
Tactile localization - normal normal
Stereognosis - normal. Normal
Graphesthesia - normal. Normal
Cerebellar examination: right left
Finger nose test - normal. Normal
Finger nose finger test- normal. normal
Disdiadokinesia - no no
Heel knee test - normal. normal
Tandom walking. - could not be performed
Rombergs sign - could not be performed
Gait examination- hemiplegic gait
Spine examination- normal
Peripheral nerves - no nerve thickening,no foot or wrist drop.
Here are some videos of her CNS examination
Other systems
CVS: S1S2 +, No murmurs, Apex normal
Respiratory system: Normal vesicular breath sounds +, no added breath sounds.
GIT : No abnormalities +
Provisional Diagnosis :
Sudden onset right sided hemiparesis which is gradually progressive, with right UMN type of Facial palsy and 3rd nerve involvement due to demyelinating/inflammatory etiology involving midbrain and Pons.
With the given history and examination we evaluated her further
MRI BRAIN (Plain and contrast) with Angiogram was done that showed
T2 weighted Transverse section MRI BRAIN showing hyperintensity involvement of Midbrain sparing Red Nucleus.
Carotid Artery Doppler: Soft Plaque in left carotid artery without significant stenosis.
ECG
The World Health Organization estimated that there were 463 million diabetics in 2019 and this number would increase to 578 million by the year 2030 and 700 million by 2045. India leads the world with largest number of diabetic subjects earning the dubious distinction of being termed the “Diabetes capital of the world”. (1) According to the Diabetes Atlas 2017 published by the International Diabetes Federation, the number of people with diabetes in India currently around 72.9 million is expected to rise to 134.3 million by 20453. Diabetic nephropathy is one of the leading causes of chronic renal failure in India. DIABETIC RETINOPATHY: In India, the previous studies to calculate prevalence were by Raman et al. (18.1%) (4), Rema et al. (17.%) (5), Namperumalsamy et al. (10.6%) (6), Narendran et al. (26.2%) (7) and Dandona et al (8). The prevalence in the AIOS study was 21.27% with a range of 12.27% in the central zone and 34.06% in the north zone.PERIPHERAL VASCULAR DISEASE: Prevalence of PAD in T2D patients in Delhi, North India, is much lower than that reported in western population (∼20%) and from south India (6.3%). Prevalence of PAD was higher in patients with higher age, longer duration of diabetes, lower BMI, and higher total and LDL cholesterol (9). CORONARY ARTERIAL DISEASE: The prevalence of CAD in the CUPS study was 11% in the total population, with 1.2% patients having had a MI, 1.3% with Q-wave changes, 1.5% with ST-segment changes, and 7.0% with T-wave abnormalities (10,11). This 11% represents a 10-fold increase in CAD prevalence in urban India since 1970 (10,12), now approaching those reported in migrant Indians. In the same study, the prevalence of CAD among diabetic subjects was 21.4% (known diabetes, 25.3%, and newly diagnosed diabetes, 13.1%), which was much higher than the figure of 14.9% among subjects with IGT and 9.1% among those with NGT. Prevalence of known MI was three times higher in diabeticsubjects. DIABETIC NEPHROPATHY: A study was performed to evaluate the various etiologies of CKD among patients presenting to the Department of Nephrology, Guwahati Medical College, a tertiary referral center. A total of 5718 CKD patients were evaluated to identify the cause of CKD. The most common cause was found to be diabetes mellitus in 42.2%, followed by chronic glomerulonephritis in 21.4%, hypertension in 19.5%, obstructive uropathy in 6.9%, chronic interstitial nephritis in 3.6%, and autosomal dominant polycystic kidney disease in 1.5% of the patients. Nearly 2.7% of the patients had CKD of unknown etiology (13). EFFECT OF SOCIOECONOMIC STATUS Prevalence of diabetes was found to be lower in low socioeconomic group living in urban areas compared with the high income group. This was probably related to the physical activity of the low income group as most of them were involved in moderate to strenuous physical activity. However long term complications like CAD, CKD, PAD and diabetic retinopathy are more common in low socioeconomic group because of uncontrolled blood sugars, alcohol and smoking. 
2D echo: normal
Chest x-ray PA view:
Treatment:
1.Iv methyl prednisolone 1gm /IV was started and continued for 5 days
2.Tab.Ecospirin Av(75/20 mg) /po/OD
3. Supportive treatment
After IV Methylprednisolone Patient improved symptomatically
And objectively her power improved in upper limbs to 4/5 and lower limbs - initially from 2/5 to 4/5 over period of 2-3 days.
This video is taken after Receiving high dose of steriods, Patient was able to walk alone for some distance, with some difficulty. But there is significant improvement in Power going by objective evidence of muscle power.
LUMBAR PUNCTURE:
Lumbar puncture was done,
1.Iv methyl prednisolone 1gm /IV was started and continued for 5 days
2.Tab.Ecospirin Av(75/20 mg) /po/OD
3. Supportive treatment
After IV Methylprednisolone Patient improved symptomatically
And objectively her power improved in upper limbs to 4/5 and lower limbs - initially from 2/5 to 4/5 over period of 2-3 days.
LUMBAR PUNCTURE:
Lumbar puncture was done,
and CSF analysis was sent.
Colur - colorless
Appearance- clear
Total counts - 16cells /cumm
Lymphocytes-100%
Neutrophils - nil
CSF glucose -94mg/dl
Protein- 79mg/dl
Chloride -114mmol/lit
High protien and lymphocyte predominant - suggestive of inflammatory process
Anti NMO antibody levels: Serum Aquaporin levels were sent and came negative
Patient was discharged and continuously followed up.
Patient improved symptomatically and is able to walk alone and able to perform her own activities.
Review MRI was done to look for any new lesions. MRI showed regression of hyperintense lesions.
Discussion:
1.https://academic.oup.com/brain/article/122/11/2171/377380
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC490512/
6: https://www.hindawi.com/journals/pri/2012/871019/
Articular involvement is characterized by nonerosive and nondeforming arthritis which often presents with monoarticular pattern, although asymmetrical polyarthritis can occur. The articular involvement is usually transient in nature with episodes lasting from a few days to weeks
Parenchymal involvement including brainstem involvement, hemispheric manifestations, spinal cord lesions, and meningoencephalitis is seen in the majority of patients (%80)
Table 6: Summary of evidence-based algorithmic therapy for Neuro-Behc ̧ et’s disease.
1st line. Corticosteroids
2nd line Azathioprine, cyclophosphamide, Anti-TNF-α, IFN-α
3rd line Methotrexate, Anticoagulation
In parenchymal involvement, corticosteroids (100 mg/d or 1 gx 5 days as pulse treatment) should be the first choice. Azathioprine is usually com- bined with corticosteroids. In severe or unresponsive cases, cyclophosphamide can be given additionally [83]. Anti-TNF- α agents and IFN-α are other new effective alternative agents [19]. Methotrexate is another treatment alternative [67, 68].
7. https://www.sciencedirect.com/science/article/pii/B9780702040887001103
Nervous system involvement, known as “neuro-BS” (NBS), is seen in about 5–10% of all cases. Clinical and imaging evidence suggests that primary neurologic involvement in BS may be subclassified into two major forms: the first, which is seen in the majority of patients, may be characterized as a vascular-inflammatory central nervous system disease with focal or multifocal parenchymal involvement, mostly presenting with a subacute brainstem syndrome and hemiparesis (intra-axial NBS); the other, which has few symptoms and a better neurologic prognosis, may be caused by isolated cerebral venous sinus thrombosis and intracranial hypertension(extra-axial NBS), occurring in 10–20% of the cases.
1.https://academic.oup.com/brain/article/122/11/2171/377380
This shows only few percent of people show Neurologic symptoms prior to systemic manifestations, and most commonly they develop within 6months - 1 year,( range 6 months -3years)
On the other hand, Ikedat7 stressed that the common neurologic features of neuro- Behqet's syndrome were motor impairment especially bilateral pyramidal signs and that the mental changes mainly consisted of loss of emotional control with relative sparing of intelligence and memory.
We performed a systematic review and meta-analysis of studies on neurosarcoidosis published between 1980 and 2016
We identified 29 articles describing 1088 patients diagnosed between 1965 and 2015. Neurosarcoidosis occurred in 5% of patients with systemic sarcoidosis. Mean age at presentation was 43 years and neurological symptoms were the first clinical manifestation of sarcoidosis in 52%. The most commonly reported feature of neurosarcoidosis was cranial neuropathy in 55%, with the facial and optic nerve most commonly affected, followed by headache in 32%. Pleiocytosis and elevated CSF protein were found in 58 and 63%. MRI of the brain showed abnormalities in 70%. Chest X-ray, chest CT, or gallium-67-scintigraphy showed findings consistent with sarcoidosis in 60%, 70% and 69%, respectively.
3. Isolated Neuro sarcoidosis:
In all patients, no extranueral sarcoidosis developed during a relatively long follow-up period (mean 58 mo). Compared with the systemic neurosarcoidosis cohort (60), isolated neurosarcoidosispatients had similar demographics and neurological manifestations with a few exceptions including a more common frequency of headache, hemiparesis, and radiculopathy, leptomeningeal involvement on brain MRI, increased cell count in cerebrospinal fluid, and a more favorable clinical outcome (P<0.05).
4: Isolated neuro sarcoidosis presenting as meningitis
The exact etiology of neurosarcoidosis is unknown and multifactorial, involving genetic predisposition and individual and environmental factors
Exposure to mildew, musty odors, pesticides, and agricultural employment have been associated with the development of sarcoidosis
Clinical manifestations of neurosarcoidosis can be found in 5–20% of cases of systemic sarcoidosis, and these symptoms can be mild or severe 5 (Table 2). About half of patients with neurosarcoidosis can present with neurologic manifestations sooner than systemic sarcoidosis is apparent
Articular involvement is characterized by nonerosive and nondeforming arthritis which often presents with monoarticular pattern, although asymmetrical polyarthritis can occur. The articular involvement is usually transient in nature with episodes lasting from a few days to weeks
Parenchymal involvement including brainstem involvement, hemispheric manifestations, spinal cord lesions, and meningoencephalitis is seen in the majority of patients (%80)
Table 6: Summary of evidence-based algorithmic therapy for Neuro-Behc ̧ et’s disease.
1st line. Corticosteroids
2nd line Azathioprine, cyclophosphamide, Anti-TNF-α, IFN-α
3rd line Methotrexate, Anticoagulation
In parenchymal involvement, corticosteroids (100 mg/d or 1 gx 5 days as pulse treatment) should be the first choice. Azathioprine is usually com- bined with corticosteroids. In severe or unresponsive cases, cyclophosphamide can be given additionally [83]. Anti-TNF- α agents and IFN-α are other new effective alternative agents [19]. Methotrexate is another treatment alternative [67, 68].
7. https://www.sciencedirect.com/science/article/pii/B9780702040887001103
Nervous system involvement, known as “neuro-BS” (NBS), is seen in about 5–10% of all cases. Clinical and imaging evidence suggests that primary neurologic involvement in BS may be subclassified into two major forms: the first, which is seen in the majority of patients, may be characterized as a vascular-inflammatory central nervous system disease with focal or multifocal parenchymal involvement, mostly presenting with a subacute brainstem syndrome and hemiparesis (intra-axial NBS); the other, which has few symptoms and a better neurologic prognosis, may be caused by isolated cerebral venous sinus thrombosis and intracranial hypertension(extra-axial NBS), occurring in 10–20% of the cases.
-------------------------------------------------------------------------------------------------
SHORT CASE- 2:
History taken from patient and his wife and is reliable
A 45 year old male, right handed, resident of buggilapuram, daily labourer presented with
chief complaints of
- fever since 10days
-difficulty in breathing since 10days
-decreased appetite since 10days
-burning micturition since 10days
History of present illness:
-Patient was apparently alright 10days back, then he had fever - high grade, continuous, associated with chills, relieved on medication
- Complaints of difficulty in breathing since 10days acute in onset, gradually progressed from grade 2 to grade 3 over 10days.
-Not associated with cough, chest pain, palpitations. Associated with orthopnea.
Not associated with PND.
-Complaints of decreased appetite since 10days.
-Complaints of burning micturition since 10days.
History of antibiotics 10days back for fever.
No history of hematuria, decreased urine output, pedal edema, facial puffiness.
No history of vomitings, loose stools, constipation.
No history of pain abdomen.
No history of joint pains or bone pains.
No history pruritis.
No history of melena, hematemesis.
No history of analgesic abuse.
Past illness: History of similar complaints of fever, burning micturition 1year back and was diagnosed as having AKI and started him on hemodialysis - 5sessions of hemodialysis done and 3 PRBC transfusions done.
Not a k/c/o Hypertension, Diabetes, epilepsy, asthma, Tuberculosis, thyroid disorder, CAD.
Family history:
No similar complaints in family.
Personal history:
Married
Mixed diet
Appetite -decreased since 10days
Bowel and Bladder habits - regular
Alcoholic - since 30yrs , daily (1beer (12gm of alcohol) and toddy)
Non smoker
Habit of beetle nut chewing since 30yrs.
Drug history : He is taking
T.SHELCAL 500mg /PO/OD
T.NODOSIS 500mg /PO/OD
T.OROFER -XT /PO/bid since 1year.
Summary :
A 45 year old male patient who is a chronic alcoholic , non hypertensive and non Diabetic presented with fever , difficulty in breathing , burning micturition since 10days .
Differential Diagnosis:
1.Acute kidney injury on chronic kidney disease
2.AKI causing Acute interstitial nephritis secondary to drug induced
3.AKI secondary to Acute interstitial nephritis due to infection.
General examination:
Moderately built and nourished
Patient is conscious, coherent and cooperative.
GCS: E4V5M6
BMI: 24.8kg/m²
Vitals:
Pulse - 95beats per minute, regular, normal volume, vessel wall normal, no radio-radial delay, no radio femoral delay, all peripheral pulses felt.
Blood pressure:
Right arm -130/70mmHg, supine position
Left arm -130/70mmHg, supine position
Right leg - 130/80mmHg
Left leg -130/80mmHg
Respiratory rate- 24cycles per minute, abdominothoracic, no usage of accessory muscles.
Temperature - 98.2F
SpO2-98% at room air
JVP - not elevated
Physical examination:
Oral cavity -staining of teeth with tobacco
Pallor +
No Icterus
No cyanosis
No clubbing
No generalized lymphadenopathy
No Pedal edema
Systemic examination:
CVS:
S1 and S2 heard
No murmurs
Apical impulse in left 5th intercoastal space in mid clavicle line.
No thrills, parasternal heave.
Respiratory system:
Normal vesicular breath sounds present
No adventitious breath sounds heard
Gastrointestinal system:
Abdomen:
scaphoid abdomen
No visible scars, sinuses and peristalsis
Umbilicus- central, circular.
Palpation - soft, non tender, no oraganomegaly
Auscultation: Bowel sounds + 6 per minute
No audible bruit
Percussion: tympanic note
Central nervous system:
Conscious, coherent and cooperative
Speech - spontaneous, naming, repetition, fluency normal
Normal gait
Cranial nerves intact.
Sensory system, motor system autonomic system- normal
Provisional diagnosis:
1.Acute kidney injury (AKI) on chronic kidney disease (CKD)secondary to Acute interstitial nephritis due to drug induced or infection, without features of uremia
2. severe Anemia
Investigations:
Hemogram:
Hemoglobin-3gm/dl
Total counts - 16200 cells/cumm
Neutrophils-90%
Lymphocyte-05%
Platelets- 2.08 lakhs/cumm
Peripheral smear - NC/NC Anemia
Blood group - A positive
Complete urine examination:
Colour -pale yellow
Albumin +
Pus cells 3-4 /HPF
RBC - nil
Renal function tests:
Urea - 468mg/dl
Creatinine - 25.9mg/dl
Uric acid - 16.4mg/dl
Calcium - 10mg/dl
Phosphorus- 11.3mg/dl
Sodium - 132mEq/l
Potassium - 5.3mEq/l
Chloride- 92mEq/l
ÀBG:
PH: 7.32
PCO2 :5.5 mmHg
PO2: 113mmHg
HCO3: 2.8mmol/L
BEB: -24.3mmol/L
O2 sat: 96.1%
USG abdomen:
Kidneys-
Right and left - normal size and increased echo texture.
B/l grade 2 RPD changes
ECG:
Chest xray:
Treatment:
1. started him on hemodialysis
2.2 PRBC transfusions
3.inj ERYTHROPOIETIN 4000IU/sc twice weekly
4.T.OROFER-Xt /PO/BD
T.SHELCAL 500MG /PO/OD
18100006005 THESIS
AUGUST 09, 2021
TITLE:
“ESTIMATED GLOMERULAR FILTRATION RATE AS A MARKER FOR EARLY DETECTION OF CHRONIC KIDNEY DISEASE IN TYPE 2 DIABETES MELLITUS”
INTRODUCTION:
Diabetes is major health issue that has reached alarming levels, today nearly half billion people are living with diabetes worldwide.
DEFINITION:
Diabetes is chronic condition that occurs when there are raised levels of glucose in blood either because of decreased insulin secretion (Type 1) or resistance to insulin action (Type 2) or combination of both.
Table- 1 Modified diagnostic criteria for diabetes
The World Health Organization estimated that there were 463 million diabetics in 2019 and this number would increase to 578 million by the year 2030 and 700 million by 2045. India leads the world with largest number of diabetic subjects earning the dubious distinction of being termed the “Diabetes capital of the world”. (1) According to the Diabetes Atlas 2017 published by the International Diabetes Federation, the number of people with diabetes in India currently around 72.9 million is expected to rise to 134.3 million by 20453. Diabetic nephropathy is one of the leading causes of chronic renal failure in India. DIABETIC RETINOPATHY: In India, the previous studies to calculate prevalence were by Raman et al. (18.1%) (4), Rema et al. (17.%) (5), Namperumalsamy et al. (10.6%) (6), Narendran et al. (26.2%) (7) and Dandona et al (8). The prevalence in the AIOS study was 21.27% with a range of 12.27% in the central zone and 34.06% in the north zone.PERIPHERAL VASCULAR DISEASE: Prevalence of PAD in T2D patients in Delhi, North India, is much lower than that reported in western population (∼20%) and from south India (6.3%). Prevalence of PAD was higher in patients with higher age, longer duration of diabetes, lower BMI, and higher total and LDL cholesterol (9). CORONARY ARTERIAL DISEASE: The prevalence of CAD in the CUPS study was 11% in the total population, with 1.2% patients having had a MI, 1.3% with Q-wave changes, 1.5% with ST-segment changes, and 7.0% with T-wave abnormalities (10,11). This 11% represents a 10-fold increase in CAD prevalence in urban India since 1970 (10,12), now approaching those reported in migrant Indians. In the same study, the prevalence of CAD among diabetic subjects was 21.4% (known diabetes, 25.3%, and newly diagnosed diabetes, 13.1%), which was much higher than the figure of 14.9% among subjects with IGT and 9.1% among those with NGT. Prevalence of known MI was three times higher in diabeticsubjects. DIABETIC NEPHROPATHY: A study was performed to evaluate the various etiologies of CKD among patients presenting to the Department of Nephrology, Guwahati Medical College, a tertiary referral center. A total of 5718 CKD patients were evaluated to identify the cause of CKD. The most common cause was found to be diabetes mellitus in 42.2%, followed by chronic glomerulonephritis in 21.4%, hypertension in 19.5%, obstructive uropathy in 6.9%, chronic interstitial nephritis in 3.6%, and autosomal dominant polycystic kidney disease in 1.5% of the patients. Nearly 2.7% of the patients had CKD of unknown etiology (13). EFFECT OF SOCIOECONOMIC STATUS Prevalence of diabetes was found to be lower in low socioeconomic group living in urban areas compared with the high income group. This was probably related to the physical activity of the low income group as most of them were involved in moderate to strenuous physical activity. However long term complications like CAD, CKD, PAD and diabetic retinopathy are more common in low socioeconomic group because of uncontrolled blood sugars, alcohol and smoking. FIGURE- 1 Recent population-based studies showing the prevalence of type 2 diabetes in different parts of India
ECONOMIC BURDEN OF DIABETES IN INDIA
A recent study showed that in India, the total expenditure on diabetes care was, on average Rs.10,000 in urban areas and Rs.6260 in rural areas. A study conducted in 2008 and 2009 found that total cost for patients without complications were Rs.4493 compared to Rs.14,692 for patients with complications (14).
FIGURE- 2 Estimated number of diabetic subjects in India
AIM OF THE STUDY:
To analyze estimated glomerular filtration rate as a marker in early detection of chronic kidney disease in type 2 diabetes mellitus.
OBJECTIVES OF THE STUDY:
To calculate estimated glomerular filtration rate in type 2 diabetes mellitus patients and categorize patients into different stages of CKD.
To calculate urine albumin /creatinine ratio to stage kidney damage.
To determine kidney damage based on eGFR and urine albumin /creatinine ratio. METHODOLOGY:
PATIENTS AND METHODS:
STUDY DESIGN: Single centre non randomized Cross sectional study
STUDY SETTING: All type 2 diabetes mellitus patients in out patients and inpatients admitted in Department of General Medicine, Kamineni institute of medical Sciences,
Narketpally.
STUDY DURATION: OCTOBER 2018 - SEPTEMBER 2020
SAMPLE SIZE : Type2 Diabetes Mellitus – 100 Patients
ETHICAL COMMITTEE APPROVAL: Obtained
PATIENT CONSENT: Informed consent was obtained
FINANCIAL SUPPORT: Nil
CONFLICT OF INTEREST: Nil
Collaborating Departments:
. Department of General Medicine; Kamineni Institute of Medical Sciences.
. Department of Biochemistry; Kamineni Institute of Medical Science
Selection of study subjects:
During the period of study 227 type 2 diabetic individuals (both inpatients and outpatients) were evaluated. Out of these 50 patients were excluded due to usage of ACE or ARB‟s, 7 patients were excluded because of urinary tract infection, 40 patients were excluded due to elevated serum creatinine >2mg/dl, 30 patients were excluded due to macroalbuminuria. After excluding 127 patients, 100 patients were left in the study group and were evaluated. Data was collected in a cross sectional way.
- Patients were initially screened with early morning urine for spot protein creatinine ratio and then based on absence of macro proteinuria by 24hr urinary protein. The test was repeated 3 times and a average of 3 was taken as absence of significant proteinuria.
- Fundus was studied with direct ophthalmoscope and assessed for retinopathy.
- Blood pressure was measured with mercury manometer and average of 6 blood pressure recordings were taken for analysis.
- Serum creatinine and blood glucose were analyzed using ERB full auto analyzer.
- Hemoglobin was estimated using coulter counter.
- Urine protein was analyzed using auto analyzer.
- Data was analyzed with MINITAB 15 statistical soft ware.
- Cross tabulation and chi square analysis was done using the variables recorded.
- eGFR was calculated using MDRD formula.
- INCLUSION CRITERIA:
- 1 Patients who are 40 years of age or older and completed a standardized interview and a detailed physical examination and classified as having type2 DM according to the American Diabetes Association (ADA).
- 2 Serum creatinine <2.0 mg.
- EXCLUSION CRITERIA:
1. Patients who are not willing for the study are excluded
2. Patients known to be microalbuminuric before antihypertensive therapy was started are not eligible for this study
3. Those who were/are on Angiotensin converting enzyme inhibitors / Angiotensin receptor blockers are excluded
4. Patients with
• urinary tract infection,
• congestive heart failure
• Malignant hypertension
• Accelerated hypertension
All the subjects in the study group were enquired about the following:
Polyuria, polydipsia, polyphagia, weight loss, chest pain, palpitations, breathlessness, pedal edema, facial puffiness, dysuria, oliguria, hematuria, pins and needles burning sensation in extremities, foot infection, amputation, diminution of vision, acute complications like DKA, hypoglycemia, hyperosmolar state, CVA, MI.
Autonomic features like absence sweating, postural giddiness, chronic diarrhea, constipation. Any history of macrovascular complications like MI, hypertension, peripheral vascular disease, retinopathy, alcohol consumption, smoking, intake of ACEI OR ARB‟S medication.
EXAMINATION:
Height
Weight
Waist circumference
Body Mass Index (BMI)
Pulse and peripheral pulses
Blood pressure (mean of 6 readings)
TABLE-4 Staging of blood pressure according to 2020 International Society of Hypertension
Global Hypertension Practice Guidelines
Postural drop of blood pressure
Retinopathy
Normal fundus
Non proliferative diabetic retinopathy
Proliferative diabetic retinopathy
Investigations:
Complete blood picture
Complete urine examination
urine albumin/creatinine ratio
Blood Glucose - Fasting blood sugar, Post lunch blood sugar, HbA1c
Blood urea: Serum creatinine: Serum electrolytes:
Fasting Lipid profile
Urine spot protein creatinine ratio
24 hrs urinary protein
MASTER CHART:
LINK TO COMPLETE THESIS WITH MASTER CHART:
https://drive.google.com/file/d/15ipE7V0Y88BHRL-z92a1HVFvriRx78Np/view?usp=drivesdk
18100006005 PROCEDURAL COMPETENCIES
AUGUST 09, 2021
PROCEDURAL COMPETENCIES
1.Performed CT Guided biopsy of Para aortic lymphnode in a 50yr old male - diagnosed as CML.
2.Performed ultrasound guided Renal biopsy in a 40yr old female with SLE
3.Placed intra arterial line in 60yr old male with necrotizing fascitis and sepsis with hypotension.
4.Placed many central venous catheters for hemodialysis during ICU posting and nephrology posting.
HALL TICKET NO. 18100006006
CASE PRESENTATIONS
AUGUST 10, 2021
LONG CASE
Chief complaints
A 28 year old male came with chief complaints of sudden fall followed by weakness of both the lower limbs (paraplegia) and loss of hand grip 10 days back, associated with bowel and bladder incontinence.
History of present illness:
Patient was apparently asymptomatic 1 month back, following which he developed productive cough, low grade fever for which he underwent sputum studies and tested positive for AFB bacilli and started ATT - HRZE regimen, 2 tab according to weight/PO/OD.
He developed generalized weakness and myalgia 15 days back.
10 days back, patient got up from bed and went to open the door and suddenly fell down, with no loss of consciousness and no froathing. Following which his brother got him up and since then Patient developed bowel and bladder incontinence.
weekness in both upper and lower limbs
lower limbs - able to move toes of bilateral lower limbs
unable to turn in the bed
unable to get from lying position
unable to walk
unable to lift his legs off the bed
upper limbs - unable to take comb to the head
unable to hold plate or glass, button or unbutton the shirt
unable to lift bucket
unable to eat food
able to move fingers and lift hand till his mouth
weekness is symmetrical and progressive.
no diurnal variation in weekness
no breathlessness, no ptosis and no facial weekness
no difficulty in chewing.
fall - no loss of counsciousness
not associated with involuntary movements,tongue bite and rolling up of eyes
not preceded by chest pain, palpitations and sweating
not associated with headache, giddiness, presyncope or visual disturbances
patient also complained of electric shock like sensation all over the body
initially he experianced shock like pain only in the neck which radiated to bilateral upper limbs when neck is flexed
and paresthesia and tingling sensation over hands
no history of disorientation, any abnormal behaviour
no speech disturbances
no loss of smell
visual acuity normal and colour vision - normal
no history of double vision and deviation of eyes to one side
no decreased or abnormal sensations over face
no difficulty in mastication
no deviation of angle of mouth, no drooling of saliva and no difficulty in closing eyes
no hearing impairment, no vertigo and tinnitus
no dysphagia, dysarthria, no nasal reguirgitation and horseness of voice
no difficulty in shrugging of shoulders
no deviation of tongue
sensory - able to feel cloths over the body
able to feel hot and cold water during bath
electric shock like sensation all over body
paresthesia and tingling over bilateral hands
bowel and bladder incontinence is seen
Past history:
He is a known case of TB since 1month and on ATT - HRZE
Not a known case of DM,HTN, ASTHMA, EPILEPSY, THYROID DISORDERS, STROKE, CAD.
Personal history:
Diet - mixed
Appetite - normal
Sleep - Adequate
Bowel and bladder incontinence + since 1 week
No allergies
No addictions
Family history:
His father is a known case of TB and used ATT for 2 years
Diagnosis;
anatomical - cervical spinal cord
functional - quadriparesis
etiological - tuberculosis
pathological - compressive extramedullary and extradural leison
General examination:
Patient is conscious, coherent, co-operative and oriented to time, place and person
No pallor, icterus, cyanosis, clubbing, koilonychia, lymphadenopathy and edema.
Temperature - afebrile
PR - 80 BPM
RR - 16 cpm
BP - 100/70 mm Hg
height - 165cm
weight - 45 kgs
BMI - 16.5kg/m2
Systemic examination:
CNS:
Higher mental functions;
patient is conscious, oriented to time, place and person, cooperative and comfortably lying on bed.
registration - normal
calculation - normal
no speech abnormalities - normal comprehension
naming of objects - normal
no writing and reading abnormalities
repetition - normal
no dysarthria
cranial nerve examination - normal
No signs of meningeal irritation
MOTOR SYSTEM EXAMINATION
lower limbs are extended at knee joint
upper limbs are in mid flexed position
bulk of muscles - symmetrical on both sides (no wasting or no hypertrophy)
Right. Left
Tone. UL. N. N
LL increased. Increased
Power UL. 4/5. 4/5
LL. 0/5. 0/5
Reflexes:
Right. Left
Biceps. 3+. 3+
Triceps. 3+. 3+
Supinator. 2+. 2+
Knee. 3+. 3+
Ankle. 3+. 3+
Plantar: extensor
SENSORY SYSTEM EXAMINATION
pin prick sensation and touch sensations are normal
pain and temperature sensations are normal
vibration sense over forehead, mastoid, clavicle, sternum, vertebral spine, tibial tuberosity and ankle is lost
joint position at great toe and thumb is absent
CEREBELLUM
no nystagmus
no intentional tremor
finger nose test, finger nose finger test and knee shin dragging tests could asses due to quadriparesis
no hypotonia
no speech abnormalities
no pendular knee jerk
no titubation
CVS:
S1, S2 heard
No thrills
No Murmurs
Respiratory system:
Trachea - central
BAE +
NVBS heard
No added
Per abdomen:
Soft, non tender
Bowel sounds - heard
Hernial orifices - normal
No palpable masses
Provisional diagnosis:
Cervical myelopathy?
Potts spine?
Investigations:
Treatment given:
1. Inj. Optineuron 1Amp in 100ml NS IV/OD
2. Inj. Thiamine 200mg in 100ml NS IV/TID
3. ATT - according to body weight 2 tab PO/OD
4. Bp/ PR/ Spo2/ Temp charting
Update:
FINAL DIAGNOSIS: Quadreparesis secondary to infectious spondylitis of C4, C5, C6, C7 and D1 with Epidural abscess at C5 - C6 level.
UPDATE:
He had surgical drainage of abcess at Osmania and getting discharged tomorrow
Outcome of intervention:
Patient regained control over bowel and bladder,
Improvement in power and tone (as he is walking now)
Adviced to continue ATT.
-------------------------------------------------------------------------------------------------
SHORT CASE- 1:
A 32 year old male patient, auto driver by occupation came to OPD with chief complaints of Pedal edema since 10 days Less urine output since 10 days
HISTORY OF PRESENT ILLNESS
The patient was asymptomatic one year ago and developed diminision of vision consulted doctor and was diagnosed with hypertension for which he has been using Tab.Arkamin and Tab.Telma H since 1 year. He developed pitting type of edema below the knee since one month, weakness and backache since one month which relieved on rest. He has decreased urine output and consumes alcohol [180ml] rarely.
HISTORY OF PAST ILLNESS
known case of CKD on MHD since 1 month
Known case of HTN since 1 year (on Tab.Arkamin, Tab Terma H)
Not a known case of DM, CAD, Asthma, TB, Epilepsy
PERSONAL HISTORY
He is single
Occupation – Daily Labourer
Diet – Mixed
Appetite – Normal
Bowels – Regular
Micturition – decreased urine output
Has no known allergies
Drinks alcohol rarely[180ml]
TREATMENT HISTORY
No specific treatment history
FAMILY HISTORY
His brother is a k/c/o HTN
DRUG HISTORY
He has been using Tab.Arkamin and Tab.Telma H since 1 year for HTN.
GENERAL EXAMINATION
Patient was conscious, coherent, cooperative and examined in a well lit room.
VITALS
Pulse rate: 98bpm
Respiratory rate: 18/min
BP: 150/80mmHg
Temperature: Afebrile
GRBS: 127mg%
SpO2: 98% at room air
PHYSICAL EXAMINATION
Pallor – absent
Icterus – absent
Cyanosis – absent
Clubbing of fingers/toes – absent
Lymphadenopathy – absent
Edema of feet – present, below the knee, pitting type.
Malnutrition – absent
Dehydration – absent
SYSTEMIC EXAMINATION
CARDIOVASCULAR SYSTEM
S1 and S2 heard
No thrills
No cardiac murmurs
RESPIRATORY SYSTEM
Vesicular breath sounds heard
Trachea is in central position
No wheezing
No Dyspnoea
ABDOMEN
Obese shaped abdomen
No tenderness
No palpable mass
No hernial orifices
No free fluid
Liver and spleen not palpable
Bowels sounds are heard
CNS
Conscious and normal speech
Normal gait
Cranial nerves normal
Sensory system normal
Motor system normal
REFLEXES
RIGHT LEFT
Biceps +2 +2
Triceps +2 +2
Supinator +2 +2
Knee +2 +2
Ankle +2 +2
INVESTIGATIons
28/07/2021
ULTRASOUND
ECG
29/07/2021
ECG 
2D ECHO
30/07/2021
HEMOGRAM
PROVISIONAL DIAGNOSIS
CKD on MHD secondary to Hypertensive nephropathy
DIAGNOSIS
Heart failure with preserved ejection fraction
PLAN OF MANAGEMENT
Renal Transplantation
Discussion is going on regarding ABO Compatibility
TREATMENT
Fluid restriction <1L/day
Salt restriction <2.4L/day
T.Lasix 40mg PO/BD
SAM – 4pm
T.Nicardia 20mg PO/TID
T.Arkamine 0.1 mg PO/BD
SHORT CASE-2:
80 year old Female who has sedentary life style without much physical activity, has been diagnosed with Hypertension 5 years back, she was put on Telma H - 40/12.5mg since then. Patient was apparently symptomatic till August 2nd night, then she experienced
Two episodes of loose stools which has foul smell, yellow in color, sticky in consistence, and there is no associated tenesmus, also experienced
Three episodes of vomiting, no odor, food particles seen, non bile stained, and non projectile
As her daughter-in-law is a pharmacist, she gave her eldoper capsule and then stools subsided but patient developed fever with chills and rigor associated with vomiting next day morning, after patient has visited Narketpally KIMS hospital where she was treated with I.V fluids, ORS, Sporolac and other symptomatic treatment
Upon enquiry she has explained us that her daily water intake used to be boiled Sagar water but on this particular day she drank Sagar water without boiling, all her family members used to drink filter water. None of the people in the same community have experienced any illness who drank Sagar water without boiling.
Patient is conscious, coherent and co-operative, heavy built and moderately nourished
Upon general examination from head to toe,
Hair is thin and grey in color
Eyebrows, eyes, nose, lips appear normal
Neck short with double chin
Truncal obesity present
Hands and legs appear normal
Vitals
BP - 90/60 mm of hg
Pulse rate - 100 bpm
Temperature - 103 degree Fahrenheit
GRBS - 126 mg/DL
Respiratory rate - 20 cycles/min
SPO2 - 96% at room
Pallor - Present
No cynosis, No clubbing, No icterus, No edema, No lymphadenopathy
Tongue dry, Skin Turgor lost, Capillary refilling time - 5secs
Systemic Examination
Cardiovascular System - S1 and S2 heard, No thrills, No cardiac murmurs
Respiratory System
Vesicular breath sounds heard
Trachea is in central position
No wheezing
No Dyspnoea
Central Nervous System
Conscious and normal speech
Normal gait
Sensory and Motor system examination - normal
ABDOMEN
Obese Abdomen is soft, non tender, No palpable mass, no organomegaly Hernial orifices - normal
Bowel sounds - Present
PROVISIONAL DIAGNOSIS - acute gastroenteritis with known case of hypertension
On the first day of admission
five episodes of loose stools, three episodes of vomiting, fever with chills, temperature 103 degree Fahrenheit
Treatment Given
IV fluids
Inj. PANTOP 40mg OD
inj. ZOFER 4mg IV SOS
T. DOLO 650mg TID
inj. MONOCEF 1gm IV BD
inj. METROGYL 100ml IV TID
T. SPOROLAC DS TID
inj. NEOMOL 1gm IV SOS (If temp > 101degree Fahrenheit)
Mix ORS Sachet in 1litre water, drink 200ml after each episode of loose stool
INVESTIGATIONS
Hb - 8.8 gm/dl
Total WBC count - 9100 cells/cumm
Neutrophils - 80%
Lymphocytes - 15%
PCV - 25.5% decreased
Platelet count - 1.76 lakhs/cumm
Serum Creatinine - 2.2 mg/DL
Blood Urea - 69 mg/DL
Sodium - 136 mEq/L
Potassium - 3.2 mEq/L
Chloride - 97 mEq/L
Total Billurubin - 1.18 mg/dl
Direct Billurubin - 0.36 mg/dl
SGOT(AST) - 24 IU/L
SGPT(ALT) - 17 IU/L
ALP - 180 IU/L
Total Proteins - 6.5gm/dl
Albumin - 3.4 gm/dl
USG
Raised echogenicity with grade-1 renal paramchymal changes in bilateral kidneys
on subsequent days of admission
frequency of loose stools increased (10 to 14) episodes in a day
vomotings and fever subsided
same treatment was continued
inj. optineuron and T. redotil were added
stool microscophy revealed few inflamatory cells
stool culture was negative
hanging drop test did'nt show any motility of organisms
hanging
QUESTIONS
Is stool culture helpful in management of acute gastroenteritis
when to start antibiotics in acute gastroenteritis
18100006006 THESIS
AUGUST 2021
TITLE
“ETIOLOGY, MANAGEMENT AND OUTCOME IN PATIENTS WITH HYPONATREMIA IN ICU KIMS, NARKETPALLY”
INTRODUCTION:
Hyponatremia is the most common electrolyte disorder among hospitalized patients and has been associated with increased mortality. Hyponatremia is defined as a serum sodium concentration (Na+) less than 135 mEq/L
Serum sodium levels and serum osmolality are normally maintained under precise control by homeostatic mechanisms involving thirst, anti-diuretic hormone and the renal handling of filtered sodium. Hyponatremia occurs in a broad spectrum of patients who are asymptomatic or critically ill.
Patients in whom the serum sodium concentration is greater than 130 mEq/L are usually asymptomatic, whereas those in whom these values are lower may have symptoms. Clinical symptoms vary from individual to individual. Majority of patients with hyponatremia are asymptomatic. Most patients with hyponatremia have non-specific symptoms or symptoms due to an underlying disease or disorder. The clinical manifestations of hyponatremia are produced by brain swelling and are primarily a function of the rate of fall of serum sodium concentration and not the absolute level. Symptoms occurring early in hyponatremia is usually anorexia, nausea, vomiting. Some patients may have headache and irritability. As serum sodium levels falls further patients develop neuropsychiatry symptoms.
These symptoms range from restlessness, altered consciousness, lethargy, seizures to coma. As the symptomatology vary markedly, the diagnosis of hyponatremia is difficult to establish. Prompt recognition and optimal management of hyponatremia in hospitalized patients may reduce in-hospital mortality and symptom severity, allow for less intensive hospital care, decrease the duration of hospitalization and associated costs and improve the treatment of underlying co morbid conditions and patients’ quality of life. So the treating clinician should have a high index of suspicion to diagnose hyponatremia.
There are serious neurological sequelae associated with hyponatremia and its management. The possible causes of hyponatremia should always be sought in every case. The presence of symptoms and duration of hyponatremia guide the treatment strategy. Thorough evaluation for hyponatremia mandates accurate history taking and clinical examination along with various investigations
AIM:
To study etiology, management and outcome in patients with
hyponatremia in ICU KIMS, Narketpally.
OBJECTIVES:
To determine the etiology of clinically significant hyponatremia in ICU patients
To study the management given to these patients
To observe the outcome in these patients
To study the various diseases associated with hyponatremia
PATIENTS AND METHODS
Place of study - Intensive Care Unit in Kamineni Institute Of Medical science
Period of study - oct 2018 – sept2020
Type of study - prospective study
Study population - 60 patients
THE LABORATORY
The Biochemistry lab is a standardized laboratory. The methods used for estimation are:
1. Serum Sodium – HILITE/Transaminase
2. Serum Potassium – I.S.ELECTRODE (Ion selective
Electrophoresis)
3. UREA – Glutaraldehyde LDH
4. Creatinine – Jaffe Kinetic
5. SUGAR – (GOD/POD/Glucose oxidase peroxidase)
6. LFT – Enzymes – kinetic
7. TFT – Automated ELISA reader
8. Urine Na – I.S.ELECTRODE
9. Urine K – I.S.ELECTRODE
10. Lipids – ENZYMATIC METHOD
INCLUSION CRITERIA:
All patients greater than 13 years of age
All patients with sodium values less than 130mmol/l
EXCLUSION CRITERIA:
Patients with age less than 13 years
Patients who are treated with mannitol and osmotic diuretics
LINK TO COMPLETE THESIS WITH MASTER CHART:
https://www.scribd.com/document/519437512/Manasa-thesis
18100006006 CLINICAL COMPETENCIES
AUGUST 10, 2021
