PG FINAL YEAR (2018-21) BATCH UNIVERSITY PRACTICAL EXAMINATION

 18100006007 CASE PRESENTATIONS

AUGUST 10, 2021

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  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 progressive 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, 

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 disturbed sleep since one month, where he complained of excessive day time sleepiness and night distured 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 pubic hair - sparse.

B/ l parotid enlargement - negative

No fetor hepaticus

No asterixis

No gynaecomastia

Spider nevi - absent

No planar erythema

No leuconchyia

Flapping tremors - seen.

Inspection - 

Oral cavity - No dental caries and no Tobacco staining

Abdomen - flanks full, distension.

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

Pubic symphysis to umbilicus - 13cms

Percussion - 

Liver span - 15.7 cm in mid-clavicular line

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. 

Child-Pugh SCORE - C

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. Serum albumin - 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.

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SHORT CASE-1:

Case:

A 43year old female came to OPD with chief complaints of:

CHEST PAIN SINCE 10 DAYS

FEVER SINCE 10 DAYS 

COUGH WITH EXPECTORATION SINCE 10 DAYS

HISTORY OF PRESENT ILLNESS:

Patient was apparently asymptomatic 10 days back and then presented with ;

Pain in the right SIDE OF THE CHEST region  ,  non radiating, increased with inspiration and coughing .

She also complained of  fever, moderate to high grade ,associated with chills and rigors ,  since 10 days. She also complained of cough with scanty mucoid expectorant which wasn't blood tinged, non foul smelling since the past 10 days

She however had no complaints of weight loss,  dyspnea, burning micturition, vomiting, diarrhea.

No history DM, HTN, CAD, CVA, Thyroid Disorders, pulmonary tuberculosis

ON EXAMINATION 

Patient was conscious, coherent, cooperative 

She was moderately built, well nourished 

She had pallor, though no signs of cyanosis, clubbing, pedal edema, lymphadenopathy,

Temperature 100.6 F.

Pulse 98 bpm, regular, normal in volume with no radioradial or radiofemoral day

BP 140/ 80mmhg checked in right arm in supine posture

RR 22 cpm

Spo2 91% on room air

GRBS - 105 mg/dl

 Respiratory system examination:

INSPECTION-

shape of the chest: elliptical

symmetry:b/l symmetry

position of trachea: central

apex beat: seen in 5th intercostal space midclavicular line

Rr-22 cpm

rhythm-regular

type- thoracoabdominal

no accessory or intercostal muscles usage .

no engorged veins over the chest and neck

no obvious spine abnormality

PALPATION- 

            all inspectory findings are confirmed.

position of trachea- central

apex beat- felt ( 5th intercostal space midclavicular line)

Movements           lt                 rt

upper thorax         N                  N

anterior                  N                N

posterior                 N               decreased

chest expansion -    N              decreased

Chest expansion              lt   rt

supraclavicular              N    N

infraclavicular                N    N

mammary                        N     decreased

Inframammary               N   decreased

axillary                             N   decreased

infraaxillary                    N   decreased

suprascapular                 N    N

interscapular                   N   decreased

infrascapular                   N   decreased

Vocal Fermitus                lt   rt

supraclavicular               N   N

infraclavicular                N   N

mammary                        N  decreased

axillary                             N  decreased

infraaxillary                    N  decreased

suprascapular                 N   N

interscapular                  N  decreased

infrascapular                  N  decreased

PERCUSSION                    lt            rt

supraclavicular        resonant resonant

infraclavicular         resonant   resonant

mammary                 resonant     dull

Inframammary        resonant    dull

axillary                      resonant   dull

infraaxillary             resonant   dull

suprascapular          resonant   resonant

interscapular           resonant    dull

infrascapular           resonant    dull

AUSCULTATION.         lt          rt

supraclavicular        nvbs    nvbs

infraclavicular         nvbs    nvbs

mammary                 nvbs    reduced

axillary                      nvbs    reduced

infraaxillary             nvbs    reduced

suprascapular          nvbs    reduced

interscapular            nvbs    reduced

infrascapular            nvbs    reduced

no added sounds

no wheeze/crepts/rub

Cardiovascular System Examination: S1 S2 heard, no murmurs 

Per Abdomen:  soft, non tender, no organomegaly

Central Nervous System Examination:

             HMF intact

 Speech normal

 Sensory system N

  Motor system N

Provisional Diagnosis:

Right sided pleural effusion 

INVESTIGATIONS

ECG:

Chest Xray PA view:

Haemogram:

Hb :9.5 gm/ dl 

TLC :17200 cells / cumm

Lymphocytes:15%

RBC : 4.12 

Plt- 3.7 lakhs cells /cumm

Smear :

Normocytic hypochromic with neutrophilia and thrombocytosis 

LFT:                                            RFT:              

                                                   BLOOD UREA:27mg/dl

 TB - 0.6 mg/ dl                         SERUM creatinine:0.8mg/dl

DB - 0.2 mg/ dl 

SGOT - 16

SGPT- 27

Alp - 239

TP-6.8

Albumin -2.9

A/G- 0.74

RBS:128mg/dl

USG ABDOMEM: normal

Pleural fluid analysis:

Pleural tap was done following all the aseptic measures, on right side 6 th posterior intercostal space, white viscous fluid was taken out and sent for analysis

CELL COUNT

Volume: 1ml

Colour: pus like material

Appearance: Cloudy

Total Count: Plenty cells/cumm

DIFFERENTIAL COUNT

Neutrophils: 86%

Lymphocytes: 14%

RBC: Nil

Others: Nil

SUGARS: #34mg/dl

PROTEIN: #4.3gm/dl

Serum Protein: 6.9g/dl

Serum LDH: 319 IU/L

 Cytology report:

Smears showed rich cellularity composed of degenerating neutrophils only against eosinophilic proteniacious background 

Impression: cytology suggestive of acute inflammatory condition.

Final diagnosis:

Type 1 Respiratory Failure due to Pleural Effusion/Empyema likely due to a bacterial infection.

Treatment:

1. IV fluids 

2. Inj Augmentin 1.2g/IV/BD

3. Inj Pantop 40mg/ IV/OD

4. Tab dolo 650mg/PO/SOS

5. Syrup Ascoril / PO/ TID 

10ml,  with one glass of water

6.iv metrogyl 500mg/iv/tid

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SHORT CASE-2:

A 18yr old male presented with complaints of difficulty in walking since 1 month

Bilateral lower limbs weakness since 15 days

Patient was apparently asymptomatic 15 days back then he gradually developed weakness in both lower limbs   which initially started with difficulty in wearing and holding footwear and then gradually ascended to involve his calf muscles, wherein he had difficulty in walking, which required support (walls). After a few days, the patient started noticing difficulty in getting up from bed, standing from a sitting position and difficulty in squatting.

H/o difficulty in climbing stairs

He also has a history of difficulty in getting up from bed. These symptoms appeared 5 days after the onset of the initial symptom. 1 day later, the patient started developing weakness in his hands, wherein he had difficulty in holding glasses, buttoning and unbuttoning of his shirt and writing. He has no history of difficulty in wearing a t-shirt. He has difficulty in mixing his food but no difficulty in taking the food to his mouth. History of buckling of knees +

No h/o difficulty in breathing 

no h/o difficulty in lifting the head off the pillow

No h/o sensory deficit in feeling clothes

no h/o sensory deficit for hot/cold sensation

no h/o tingling and numbness in UL & LL

no h/o band like sensation

no h/o low backache

no h/o trauma 

no h/o giddiness while washing face

no h/o cotton wool sensation

no h/o urgency/hesitancy/increased frequency of urine

no h/o urinary incontinence

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 during drinking water

no h/o fever/neck stiffness

Past history:

no h/o similar complaints in past

not a known case of DM/HTN/EPILEPSY/CVA/CAD

personal history:

mixed diet with normal appetite and normal bowel/bladder movements

h/o alcohol since 2y weekly twice.

No h/o smoking

no significant family history.

General examination:

Moderately built;poorly nourished

afebrile

Pallor present 

Icterus negative

No cyanosis, clubbing, lymphadenopathy, Edema.

no short neck

no scars;no h/o tropic ulcers

no neurocutaneous markers

BP: 100/60 mmhg

PR: 80 bpm

CVS: s1 s2 hears no murmurs

RS: bae + nvbs hears

P/A: soft, nontender

CNS:  HMF- patient conscious

oriented to place/time/person

no h/o aphsia/dysarthria

no h/o dysphonia

no h/o memory loss

no h/o emotional lability

cranial nerves- intact

MOTOR SYSTEM 

                                           Right.         Left

Bulk:                                  Normal     Normal

Measurements             U/l   28.5cm.   28.5c

                                         L/L 37 cm    37 cm

Tone:               Wrists      Hypotonia    Hypotonia

                      Biceps     Normal        Normal

                         LL.         hypotonia.      hypotonia

Power              Distal Muscle Group (Wrists) 40%.              40%

             Proximal Muscle Group (Both Extensors and Flexors) 3/5        3/5

              Distal Muscle Group (Both Extensors and Flexors) 4/5              4/5

Reflexes.  

   Superficial reflexes

                       Right.           Left

Abdominal.      Absent          Absent

Plantar            mute           mute

cremasteric.    +                +

    Deep tendon reflexes 

                     Right.             Left

Biceps.          Present         Present

Triceps.         Present         Present          

Supinator.     ---                    ---

Finger Flexor ---                    ---

Knee              ---                    ---

Ankle.            ---                    ---

SENSORY SYSTEM 

                                    RIGHT.           LEFT

SPINOTHALAMIC 

             crude touch.   N.                   N

                 pain.             N.                   N

            temperature.   N.                   N

post:

             fine touch.      N.                   N

             vibration.        N.                   N

     position sensor.    N.                   N

 cortical 

 2 point discrimination N.                   N

tactile localisation.        N.                   N

CEREBELLUM - Normal Examination

INVESTIGATIONS

HEMOGRAM: 

HB            10.4gm/dl

Platelets 2.56lakhs/cumm

TLC            10400 cells/cumm

lymphocytes 10%

smear -microcytic hypochromic anemia

 serum electrolytes

Na+ 143 meq/l

k+.    3.9meq/l

cl-.       95meq/l

CHEST X-RAY-

                                          

ECG:

                                        

Diagnosis

Bilaterally Symmetrical Ascending Proximal > Distal LMN Type Quadriparesis due to Peripheral Neuropathy upto level C7 likely due to Guillian Barre Syndrome (Acute Inflammatory Demyelinating Polyneuropathy)

Investigations - Nerve Conduction Studies.

18100006007 THESIS

AUGUST 10,2021

TITLE:

“CLINICAL PROFILE, MANAGEMENT AND OUTCOME IN PATIENTS WITH POISONOUS SNAKE ENVENOMATION” 

INTRODUCTION:

Snake bite is a common emergency encountered in the tropical and subtropical countries which are abound with dense vegetation and vast tracts of agricultural land. India has always been known as the land of exotic snakes. Of 3000 species of snakes known to the world, in India, we have around 216 species, out of which 52 are known to be poisonous. In our country, the estimated snake bite deaths are around 30,000 per year. 1 The highest incidence is in Tamil Nadu, West Bengal, Maharashtra, U.P and Kerala. 2 Due to the prevailing climatic conditions and due to the fact that a major portion of the population is rural, with vast agricultural fields, snake bite is a major health problem. Though the village population is at a greater risk, the urban and suburban are not always spared. The latter can be attributed to unhygienic city dwelling, harbouring rodents. In developing countries most of the snake bites occurs to the agricultural workers during their work in the fields. In developed countries, most common victims are adolescent and young adults due to their risky behaviour. The term venomous and poisonous are not the same. “Venomous” indicates organisms producing toxic material in the specialized gland and injecting through bite specialized venom apparatus and other means. “Poisonous” refers to detrimental effects produced by touching or consuming plants/organisms. Poison is found throughout the organisms but venom is produced in isolated glands. Most of the world‟s medically significant snakes belong to 4 families – Vipiridae, Elapidaec, Colubridae and Atractaspidinae. More than 95% of snake bites occurs over extremities. Snake venoms are complex mixtures of proteins including enzymes and Low Molecular Weight polypeptides. The fear of snake bite itself produce symptoms like nausea, vomiting, diarrhoea, cold clammy skin, syncope regardless of the injection of venom. 3 In general, Viper bites cause deleterious effects on almost any organ system. Russell‟s viper is implicated in causing Acute kidney injury and neurotoxicity apart from the usual local signs and coagulation abnormalities. In contrast, Elapidae family cause more neurotoxic manifestations with little or no envenomation. Exceptions are African pitting cobras (member of Elapidae family) produce little or no neurotoxicity but cause severe tissue necrosis and vipers like southern pacific rattlesnake (Crotalus oreganus helleri), Timber rattlesnake (Crotalus horridus horridus), Western Diamond Black Rattlesnake (Crotalus atrox), and Mohave rattlesnake (Crotalus scutulatus) produce significant neurotoxicity. Krait bites are commonly painless and produce neurotoxicity which won't resolve following administration of ASV or anticholinesterase because of post synaptic blockade. Sea snakes produce generalized rhabdomyolysis later leads to respiratory failure. 4 Envenomation of various poisonous species present varied clinical pictures for appropriate scientific management, which is getting hampered by non-scientific natural treatment resulting in deaths and disabilities. Currently, intense work is being done on the pharmacological, pathophysiological, toxicological and immunological aspects of snake venoms to develop an appropriate evidence based treatment to the snake bite victim. Hence this study was conducted at Department of General Medicine, Kamineni Institute of Medical Sciences, Narketpally to document and comprehensively analyse various aspects of snake bite envenomation cases.

AIMS AND OBJECTIVES

AIM:

The aim of the present study is to study the clinical profile, management and

outcomes in patients admitted with poisonous snake envenomation.

OBJECTIVES:

 To study the clinical profile of poisonous snake envenomation cases in KIMS, Narketpally.

 To categorize type of snake Envenomation from clinical signs and symptoms

and investigations.

 To study the outcome in terms of morbidity and mortality.

MATERIALS AND METHODS:

A single-center prospective study was conducted from October 2018 till the end of

September 2020 in the department of General Medicine, Kamineni Institute of

Medical Sciences, Narketpally, on patients admitted with snake bite envenomation.

Study design – Prospective observational study

Study place – Dept. of General Medicine, Kamineni Institute of Medical Sciences, Narketpally

Study period – 24 months (October 2018 to September 2020)

Sample size – 100 patients

INCLUSION CRITERIA:

All patients with history of snake bite with fang marks and signs of envenomation.

EXCLUSION CRITERIA:

 Patients without signs of envenomation.

 Patients admitted with unknown bite.

 Patients not willing for consent for the study.

LINK TO FINAL THESIS WITH MASTER CHART:

https://drive.google.com/file/d/16qSs2TG5-YxH6oB0t9EpYudZK2FtUIPL/view?usp=drivesdk

https://youtu.be/Ba058hFnvE8

HALL TICKET NO. 18100006008

CASE PRESENTATIONS

AUGUST 10, 2021

LONG CASE: 

A 55 year old male patient mechanic by occupation resident of kondapakagudem brought to Casualty on 4.8.2021 with complaints of h/o decreased urine output since 3 days 

HOPI:

Patient was apparently asymptomatic till 15 days back (20.7.2021) he developed shortness of breath which is sudden in onset for which he was taken to hospital. There he was given oxygen and evaluated. The doctors found that his serum creatinine levels are elevated and advised him dialysis. On 26.7.2021 while patient is being prepared for central line catheter he suffered with cardiac arrest and was resuscitated. His 1st dialysis was done on 26.7.2021. And on 26th doctors performed synovial fluid aspiration for bilateral knee joint swelling. They aspirated around 150 ml of fluid. Again same procedure performed on 30.7.2021 and drained 80 ml of fluid from right knee joint and 50 ml from left knee joint. He underwent 6 dialysis from then onwards and he taken to home after 6th dialysis. After going to he developed decreased urine output and for that reason he brought to our Casuality on 4.8.2021.

PAST HISTORY:

           Patient had history of fall from a pole in 1997. He suffered with injuries to left upper limb, lower limb, hip joint and rib cage. For which he started using pain killers till 1 month back.

 6 years back he started developing pedal edema in bilateral lower limbs, pitting type extending upto both the knees. He had h/o trauma 1 month back to right ankle due to bike accident. Swelling of right ankle with discoloration present.. 

Patient is not a known case of 

HTN, DIABETIS MELLITUS, TB, ASTHMA, EPILEPSY, CAD... 

PERSONAL HISTORY:

Diet is mixed. 

Appetite is normal. 

Sleep is adequate. 

Bowel movements are normal.

Bladder- decreased urine output. 

Addictions - history of alcohol intake since.                past 25 years. Occasionally alcoholic.

FAMILY HISTORY: 

No history of similar complaints in the family 

DRUG HISTORY: -

Patient was using painkillers (?NSAIDS) for joint pains. 

He used antibiotics outside for ankle swelling. 

SUMMARY: 

     A 55 old male patient mechanic by occupation and occasionally alcoholic brought to the Casuality with a complaint of decreased urine output since 3 days who was on dialysis. Patient has a long standing history of using painkillers for his joint pains.

GENERAL PHYSICAL EXAM:

Patient is conscious, coherent, and cooperative 

No signs of pallor, icterus, cyanosis and lymphadenopathy

Clubbing is present 

Edema is present in bilateral lower limbs, pitting type and extended upto knee joints.

 Left lower limb ankle joint swelling is present. Discoloration present and warmth to touch.

           VITALS:

PR =93 bpm

BP =120/80 my Hg

RR = 24 cpm

GRBS =136 mg/ dl

TEMPERATURE =98.6 F

SPO2= 98% on 4 lit of O2.

SYSTEMIC EXAMINATION:

CVS- S1,S2 +, no murmurs 

Jvp - not elevated 

RS- BAE+,
       B/L inspiratory crepts in ISA and IAA
P/A- Soft, NT, bowel sounds present
CNS-NAD 

DIAGNOSIS:

RENAL AKI (ATN) ON CKD ANALGESIC NEPHROPATHY WITH UTI (FUNGAL ETIOLOGY) RIGHT LOWERLIMB CELLULITIS 

HFpEF 

CHOLELITHIASIS

?ASYMMETRICAL RHEUMATOID ARTHRITIS. 

INVESTIGATIONS:

ABG:

PH=7.36

PCO2=44.4

PO2=73.8

HCO3=24.9

St HCO3=24.4

O2 Sat=92.1

RBS= 136mg/dl

BLOOD UREA= 75mg/dl->87mg/dl

SERUM CREATININE = 5.4 mg/dl->5.8mg/dl

SERUM ELECTROLYTES :-

Sodium= 131 mEq/L->132mEq/L

Potassium =3.4 mEq/L->3.5mEq/L

Chloride = 94 mEq/L->95mEq/L

LFT:

Total bilirubin = 1.29 mg/dl

Direct bilirubin = 0.28 mg/dl

SGOT = 21 IU/L

SGPT = 10 IU/L

ALP = 636 IU/L

Total proteins= 6 g/dl

Albumin = 2.6 g/dl

A/G = 0.78

HEMOGRAM:

Hb=8.1 g/dl->7.7g/dl

TLC = 18,000 ->14,800

N=84%->75%

L=6%->15%

E=2%

M=8%

PCV= 24.9

MCV= 96.1

MCH =31.3

MCHC=32.5

RBC = 2.59 millions/cumm

Platelets=  4.1 lakhs->4.37lakhs

PT= 16sec

INR= 1.11

BGT= O+

APTT=33 sec

CUE :

 Color- slightly brownish

Appearance- slightly cloudy

Reaction- acidic

Albumin- +++

Sugar- nil

Bile salts- +

Bile pigments- +

Pus cells- plenty

Epithelial cells- 1-2

RBC- 8-12

Others- fungal hyphae seen.

USG ABDOMEN:

Cholelithiasis

Increased anteroposterior diameter of kidneys with CMD - partially lost, altered echotexture.? AKI on CKD.

2D ECHO:

Mild global hypokinesia

EF= 52

Mild LV dysfunction 

IVC size - 1.6cm (mild dilated).

X-RAY OF BOTH HANDS:

X-RAY KNEE JOINTS:

CHEST X-RAY:

ECG ON THE DAT OF ADMISSION:

TREATMENT:

DATE- 4.8.2021

Inj. Piptaz 4.5g IV/Stat -> 2.25g IV/TID

Tab. Fluconazole 100mg PO/OD

Fluid restriction <1lt/day

Protein powder 2tbsp in 100ml milk daily

Temparature charting 4th hrly

PR, BP, SPO2, GRBS monitoring 2nd hrly 

DATE-5.8.2021

Fluid restriction <2L/day

Salt restriction <2g/day

Inj. Piptaz 2.25g IV/TID

Inj. Pan 40mg IV/OD

Inj. Lasix 40mg IV/BD

Tab. Fluconazole 100mg PO/OD

Protein powder 2tbsp in 100ml milk BD

Temparature charting 4th hrly

PR, BP,SPO2, GRBS monitoring 2nd hrly 

-------------------------------------------------------------------------------------------------

SHORT CASE-1:

42 year old male patient came to casualty with chief complaints of bilateral pedal edema (pitting type)(l>r) since 15 days, Fever and SOB since 2 days.

HISTORY OF PRESENT ILLNESS:

The patient was asymptomatic 15 days back until he had bilateral pedal edema(pitting) extending upto shin of tibia.

He had an ulcer over left malleoli 10 days back followed by increased swelling of left lower limb.

From the past two days he complains of low grade intermittent fever with generalized weakness and shortness of breadth (grade 2-3).

No h/o pain abdomen, vomiting, loose stools

No h/o cough, chest pain

No h/o decreased urine output/ burning micturition and no other complaints 

HISTORY OF PAST ILLNESS:

Not k/c/o DM, hypertension, asthma, epilepsy, Heart disease or tuberculosis 

PERSONAL HISTORY:

He has been consuming alcohol 180ml daily and khaini 2-3 per day for the past 20 years.

GENERAL EXAMINATION:

The patient is conscious

Icterus is present

Pedal edema is present 

Absence of pallor, cyanosis, clubbing, lymphadenopathy 

VITALS:

1.Temperature: 98.6 F

2.Pulse rate: 110 beats per min

3.Respiratory rate: 18 cycles per min

4.BP: 100/70 mm Hg

SYSTEMIC EXAMINATION:

A.CARDIOVASCULAR SYSTEM:

• S1, S2 heard
• No murmers
• Apex beat visible
• Diffuse shifted down and out
• Palpable p2
• Parasternal heave is present( grade 3)

B.RESPIRATORY SYSTEM:

• Barrel shaped chest
• BAE +
• Crepts + right sided lung fields  

                            BARREL SHAPED CHEST

       

AP diameter-23 cns, Transverse diameter-23 cms

C.EXAMINATION OF ABDOMEN:

Soft, non tender

D.CENTRAL NERVOUS SYSTEM:

No Focal Neurological Deficit

PROVISIONAL DIAGNOSIS: 

  HFref 2° to CAD    b/l PLEURAL EFFUSION

AKI ( ? prerenal )    CRS -1 

? ALCOHOLIC LIVER DISEASE

R. LOWER LOBE PNEUMONIA

? COPD 

LEFT LOWER LIMB CELLULITIS.

INVESTIGATIONS:

Investigations on 1/7/21:

Chest X-ray 

LIVER FUNCTION TESTS:

Total bilirubin -2.60 mg/dl

Direct bilirubin-1.35 mg/dl

AST-75 IU/L

ALT-31 IU/L

ALP- 157 IU/L

total proteins-6.1 g/dl

Albumin 3.5 g/dl

A/G ratio 1.37.

Serum creatinine -2.1 mg/dl

Blood urea - 81 mg/dl 

Serum electrolytes -

     Sodium - 129 mEq /L

     Potassium -4.8 mEq /L

     Chloride - 94 mEq /L

HEMOGRAM -

hemoglobin -10.3 g/dl

Total counts -19400 cells /cumm

Neutrophils-92 %

Lymphocytes -4%

Platelets -1.83 lakhs

Smear -

RBC- microcytic hypochromic 

WBC-neutrophilic leukocytosis

PLATELETS -adequate 

CUE-

 ALBUMIN -2+

sugars - nil

Pus cells - 4-6 

 USG ABDOMEN -

 bilateral pleural effusion -right > left 

 Mild ascites

 Left kidney - raised echogenicity 

2d Echo -

 Right atrium, right ventricle, left atrium -Dilated 

 Left ventricle - global akinaesia 

 EF - 30%

IVC - dilated 

ECG-

Investigation on 3/7/21:

                                    

ecg - atrial fibrillation, irregular RR interval 

 Investigations on 5/7/21:

ECG-

Hemogram:

Hemoglobin - 10.9 g/dl

Total count - 17800 cells/cumm

Platelets - 1.13 lakhs 

Blood urea - 86 mg/dl

Serum creatinine - 1.5 mg/dl

Serum electrolytes -

  Sodium - 130 mEq /l

  Potassium - 3.7 mEq/l

  Chloride - 88 mEq /l

TREATMENT: 

Treatment on 2/7/21: 

1)Fluid restriction   <1Lit / day 

2)Salt restriction <2gm /day 

3)Injection ceftriaxone  1gm IV /BD

4) Tab LASIX 40mg BD ( 8am to 4pm) 

5) Tab MET-XL 12.5 mg BD

6) BP PR temp spO2 monitoring 

7) Tab AZITHROMYCIN 500mg OD 

8) Tab ECOSPIRIN -AV 75/20 mg OD

Treatment on 3/7/21:

1)Fluid restriction   <1Lit / day 

2)Salt restriction <2gm /day 

3)Injection ceftriaxone  1gm IV /BD

4) Tab LASIX 40mg BD ( 8am to 4pm) 

5) Tab MET-XL 12.5 mg BD

6) BP PR temp spO2 monitoring 

7) Tab AZITHROMYCIN 500mg OD 

8) Tab ECOSPIRIN -AV 75/20 mg OD

Treatment on 4/7/21: 

1)Fluid restriction <1lit/day 

2)salt restriction. <2gm/day 

3) Inj. ceftriaxone 1gm IV/BD 

4)Tab LASIX 40mg BD (8am to 4pm)

5) Tab MET-XL 25mg BD 

6) Tab AZITHROMYCIN 500mg OD

7)Tab ECOSPIRIN-AV 75/20 mg OD

8)BP ,PR, temp ,spO2 monitoring 

9) tab DIGOXIN 0.25 mg stat 

Treatment on 5/7/21 : 

1)Fluid restriction <1lit/day 

2)salt restriction. <2gm/day 

3) Inj. ceftriaxone 1gm IV/BD 

4)Tab LASIX 40mg BD (8am to 4pm)

5) Tab MET-XL 25mg BD 

6) Tab AZITHROMYCIN 500mg OD

7)Tab ECOSPIRIN-AV 75/20 mg OD

8)BP, PR, temp, spO2 monitoring 

9) tab DIGOXIN 0.25 mg stat 

Treatment on 6/7/21:

1)Fluid restriction <1lit/day 

2)salt restriction. <2gm/day 

3) Inj. ceftriaxone 1gm IV/BD 

4)tab LASIX 40mg BD (8am to 4pm)

5) Tab MET-XL 25mg BD 

6) Tab AZITHROMYCIN 500mg OD

7)Tab ECOSPIRIN-AV 75/20 mg OD

8)BP PR temp and spO2 monitoring

9) tab DIGOXIN 0.25 mg stat 

10) Inj. CLINDAMYCIN 600mg IV/TID.

Treatment on 7/7/21: 

1)Fluid restriction <1lit/day 

2)salt restriction. <2gm/day 

3) Inj. ceftriaxone 1gm IV/BD 

4)tab LASIX 40mg BD (8am to 4pm)

5) Tab MET-XL 25mg BD 

6) Tab AZITHROMYCIN 500mg OD

7)Tab ECOSPIRIN-AV 75/20 mg OD

8)BP PR temp and spO2 monitoring

9) tab DIGOXIN 0.25 mg stat 

10) Inj. CLINDAMYCIN 600mg IV/TID .

-------------------------------------------------------------------------------------------------SHORT CASE-2:

A 45 year old male farmer by occupation resident of Ramannapet brought to the Casualty with involuntary movements of both upper limb and lower limb on 7.8.2021.

H/O PRESENT ILLNESS:

45 year old male patient had involuntary movements of both upper limb and lower limb since morning, 3 episodes and each lasted for 2 to 3 mins. Associated with up rolling of eye balls, loss of consciousness and tongue bite. H/o 3 episodes of vomitings after episode. Post ictal confusion is present. No Involuntary defecation and micturition. No h/o fever. 

PAST HISTORY:

Patient had similar episodes 3 years back. He had loss of consciousness, tongue bite, uprolling of eye balls and was under alcohol effect. MRI brain was done at that time and it was normal. 

H/o jaundice 3 years back 

K/c/o Diabetes mellitus since 3 years and on regular medication. 

Not k/c/o htn, asthma, TB and thyroid disorders 

TREATMENT HISTORY:

Tablet GLIMY M1 once daily for DM.

 PERSONAL HISTORY:

Diet is mixed 

Appetite normal 

Bowel and bladder - normal

Addictions- 

       Alcoholic since 20 years 

         90 ml per day initially 

         Now 360 ml /day 

        He experiences sleep disturbances, tremors, palpitations if doesn't consume alcohol 

        Tobacco chewing since 6 years. 2 - 3 packets per day.

FAMILY HISTORY: Nil significant 

GENERAL EXAMINATION:

                  Patient is conscious, coherent, cooperative 

 Moderately built and nourished 

No palor 

No icterus 

No cyanosis

No clubbing 

No koilonychia

No lymphadenopathy

No edema 

Vitals:

PR-84 bpm

BP- 140/80 mmhg

RR-20 cpm

SPO2-98% at room air 

GRBS-70 mg /dl at the time of admission 

SYSTEMIC EXAMINATION:

CNS:

1.Higher mental functions- 

      Patient is lethargic

      Memory -intact 

      Oriented to time, place, person.

      Speech- normal

2. Cranial nerves -

       All cranial nerves are intact. 

       No abnormality detected. 

3. Motor system -

      No wasting of muscles

     Tone - normal

      Power - upper limb 5/5

                     Lower limb 5/5

4.sensory system 

       No abnormality detected. 

5. Reflexes- 

                                    U/L.        L/L

     Biceps.                    2+           2+

     Triceps.                   2+.          2+

     Supinator.              2+          2+

     Knee jerk.               2+          2+

     Ankle jerk.              2+          2+

5. Cerebellar function - normal 

6.Gait - no abnormality. 

CVS:

      No visible pulsations seen over chest

      Jvp -not elevated

      S1 S2 +

      No added sounds heard 

 RESPIRATORY SYSTEM:

    bilateral air entry present

   Breath sounds - normal

GIT:

    Abdomen - soft and non tender

    No hepatomegaly

   No spleenomegaly

    Bowel sounds - normal

Provisional diagnosis:

    Generalized tonic clonic seizures secondary to metabolic cause 

(? Hypoglycemia ? Acute intoxication of alcohol) 

Investigations:

1)Rft-

Urea-25 mg/dl

Creatinine -0.8 mg/dl

Uric acid- 9.2mg/dl

Calcium - 10.1 mg/dl

Phosphorous - 3.7 mg/dl

Sodium -134 meq/l

Potassium -4 meq /l

Chloride - 97 meq/l

2) liver function tests -

Total bilirubin -2.64 mg/dl

Direct bilirubin-0.42 mg/dl

AST - 32 IU/L

ALT-15 IU/L 

ALP - 200 IU/L

total proteins- 7.2 g/dl 

Albumin-3.9 g/dl

A/G ratio 1.24.

3) USG ABDOMEN-no abnormality detected

Treatment given:

1) inj.LEVIPIL 500 me iv bd

2) inj. THIAMINE 1 amp in 100 ml NS iv tid.

3) inj.optinueron 1 amp in 100 ml NS iv od

4) inj. PAN 40 mg iv od

5) inj. ZOFER 4 mg iv tid

6) inj. LORAZ 2 CC iv sos

7) inj dextrose 5% iv @100 ml per hour 

8)grbs monitoring 2nd hourly 

9)BP/ PR/TEMP/SPO2 monitoring. 

18100006008 THESIS

AUGUST 10, 2021

TITLE:

“ASSESSMENT OF LEFT VENTRICULAR FUNCTION IN ISCHEMIC STROKE

INTRODUCTION:

Heart disease is a major risk factor for stroke, ranking third after age and hypertension1. 

Congestive Cardiac failure ranks second in cardiogenic stroke risk1 with a two to three fold relative risk1,2

Heart failure is a progressive and debilitating disease, is increasing in epidemic proportions and affecting both the developed and the developing world3,4.

Heart failure is associated with shorter life expectency, increased frequency of hospitalization and poor quality of life, and is a major public health challenge even in India5-8.

In order to reduce the complications of heart failure it is essential to diagnose and treat pre symptomatic left ventricular dysfunction (LVD). We focus on a new way to screen for asymptomatic LVD which is likely to be cost-effective.

LVD is a treatable condition, which accounting for 8% of people aged 25–75 years, 12% of 45-75 years old. Of the 8%, 4% are asymptomatic9.

The patients who appear to be at high risk of LVD are those with ischemic heart disease, hypertension or diabetes, and smokers10-12 But, the echocardiographic screening of all these patients for left ventricular dysfunction is a costly process. So, one can screen the patients who have their first vascular episode. 

The first vascular episode could be either a myocardial infarction (MI), a transient ischemic attack (TIA), a cerebrovascular accident (CVA) or peripheral vascular disease.

In most of TIA/CVA/PVD patients, the cause of death is a cardiac problem. So, screening of these patients with ECG and echo after their first vascular episode could be helpful to identify the underlying cardiac issue like LVD. So that one can treat it and reduce the subsequent overt heart failure and even sudden cardiac death.

So, in this study, I have tried to assess left ventricular (LV) function in patients, presented with ischemic stroke.

AIMS AND OBJECTIVES:

To study left ventricular function in ischemic stroke patients by electrocardiogram

(ECG) and echocardiogram (2D ECHO).

PATIENTS AND METHODS:

STUDY DESIGN: Cross sectional study.

STUDY SETTING: All patients admitted with ischemic stroke in Department of

General Medicine, Kamineni Institute of Medical Sciences, Narketpally.

STUDY SAMPLE: 100 patients with ischemic stroke.

PERIOD OF STUDY: 2 years from October 2018 to September 2020.

INCLUSION CRITERIA:

• Age more than 40 yrs

• Patients diagnosed with ischemic stroke by using CT/MRI BRAIN screening.

EXCLUSION CRITERIA:

• Patients under the age of 40 yrs will be excluded from the study group.

• Patients with haemorrhagic stroke will be excluded from the study group

METHODOLOGY

• ECG, 2D-ECHO, CT/MRI BRAIN will be performed in all study patients.

• Repeat CT/MRI brain after 48hrs if initial scan is normal.

INVESTIGATIONS:

• Complete blood picture

• Complete urine examination

• Blood urea, Serum creatinine, serum electrolytes

• Fasting lipid profile

• Carotid Doppler

• Chest X-ray.

• ECG

• 2D-ECHO

• CT/MRI BRAIN

MASTER CHART:

https://docs.google.com/spreadsheets/d/16D3SIbC7UPjbRiZt2Y9538xgzSCcQq5E/edit?usp=drivesdk&ouid=108872713690900170464&rtpof=true&sd=true

LINK TO COMPLETE THESIS WITH MASTER CHART:

https://drive.google.com/file/d/169kfAxkum1-sg0u4Gnh2aPBTO7N6Qpem/view?usp=drivesdk

https://youtu.be/Np7VznILFO8

HALL TICKET NO. 1800006009

CASE PRESENTATIONS

AUGUST 10, 2021

LONG CASE: 

Informant: Patient 

A 38 year old male, a resident of Chandanapally, Nalgonda district came to the hospital with complaints of difficulty in walking since 8 years

Chief complaints: difficulty in walking since 8 years (2014 March)

Feeling weak during walking since 7 years (2015 January)

History of present Illness: The patient had difficulty while walking, while getting up from chair without support, but gets up from chair with support, difficulty in squatting, difficulty in sitting on floor, difficulty in getting up without support from floor.

Initially he had difficulty in going uphill but since 3 years he was complaining of difficulty in walking on level ground also. 

      Uphill: steps are difficult 

      Downhill: comparatively easier steps than uphill

Difficulty in running 

The patient did not have any difficulty in wearing chappals, holding chappals. He did not have any problem in removing chappals. However he complained that it was easier to walk without chappals since there was lesser weight lifting needed. 

After having these symptoms for 8-9 months the patient went to the hospital for checkup and was given medication for which there is no record of with the patient. According to the patient, he was not on regular medication and the medication didn’t improve his symptoms.

Overtime, he had feeling of heaviness of upperlimb while lifting his hand over the head which progressed over time to having difficulty in lifting his arm to shake hands, eat his food and take his brush from the cupboard. He complains that he has to give an increased initial try for him to lift his hand.

After initiating combing, he doesn’t have any difficulty in combing the hair. He feels that it is difficult to move the brush in his mouth.

Difficulty in lifting food to mouth. Not associated with falling of food particles and not associated with falling of food from mouth. No difficulty in chewing food after putting food in the mouth.

Difficulty in bathing with mug. Washes more on the right side with difficulty in washing on the left side. 

Difficulty in getting from bed without support since 1 year. No difficulty in turning to sides on bed.

No difficulty in eating, chewing, closing eyes, swallowing food, whistling, shouting, winking.

Complaints of intermittent spasm of muscles after prolonged sitting. Complaints of muscle cramps. 

No complaint of difficulty in feeling things he touches. No difficulty in feeling chappals sensation. As he walks without chappals he is used to pain while walking and says that his feet are more prone to injuries.

He doesn’t have any difficulty in feeling pain when there is an injury. He doesn’t have ulcerations or abnormal sensations anywhere on the body.

He is able to feel the temperature of the water while bathing. 

The patient doesn’t have any complaints of blurring of vision, difficulty in smell, double vision, vision difficulties, no loss of area of vision, no difficulty in swallowing and tasting, normal facial expressions, no difficulty in hearing sounds of low intensity or high intensity.

No difficulty in turning head, no difficulty in eating or drinking.

No history of loss of consciousness, no irritability to light or sound, no loss of memory, no abnormal visions, sounds, the patient does not use spectacles.

The patient complains the he feels bad that he lost his job as a watchman because of the difficulty in working after onset of difficulty in walking and weakness. But he does not have history of acting out. He feels bad about not earning money but he tells that he got used to the complaints over time.

No history of headaches, nausea, vomiting, involuntary movements.

The patient does not complain of loss of balance or falls but he tells that sometimes while getting up from a chair, he doesn’t have the power to get up and sits back.

No complaints of urgency, hesitancy, increase in frequency during night, difficult in initiating urination, burning during urination.

He had complaints in difficulty in passing stools intermittently for which he takes more water or a tablet and the symptom subsides. He didn’t contact doctor for the complaint as it was intermittent and reduced with more intake of water and bananas.

No history of fever, sleep disturbances, no history of injury to feet.

Birth history: The patient had history of second degree consanguinity and was born at home with the help of dai and apparently without any problem after birth in his words. 

He walked without support at 3 years and started talking in sentences at 7 years of age. He has stuttering while talking but doesn’t have a problem in formation of sentence, language or difficulty in pronunciation of words. He says that he stutters more when there is lack of sleep.

Family history: No history of similar complaints in the family. His mother and father died in an accident and he is not married due to his stuttering problem at first and weakness later.

Personal history: The patient was a smoker previous for 6 months in 2012 but stopped later. 

He is an occasional alcoholic and drinks one glass of toddy during festivals. No sleep and appetite abnormalities. No bowel and bladder abnormalities.

Past history: The patient had a history of fall from cycle in 2012 after which he had a fracture in the left wrist but did not go to the hospital and took Ayurveda treatment. Now there is a deformity in the left wrist and reduced range of movement with difficulty in using the hand. 

No known history of diabetes, hypertension, bronchial asthma, allergies, tuberculosis, jaundice or prolonged hospital stay.

Drug history: No known usage of drugs for more than 1 week, no history of usage of injections in the hospitals. No known history of any drug allergies. 

Summary: Based on the above history the patient had slowly progressive weakness of the lower limbs more proximal than the distal and overtime it progressed to the upper limbs with more proximal weakness than distal and he developed weakness in the trunk overtime. He doesn’t have spasticity or rigidity in the muscles. He doesn’t have sensory complaints. He complains weakness more in the lower limbs than upper limbs. He has no cerebellar, autonomic system, cranial nerves or higher mental function abnormalities. The patient had history of consanguinity, delayed milestones and history of malunited left wrist fracture.

General physical examination: The patient is conscious, coherent, comfortable, cooperative. No distress or features of pain. The patient doesn’t appear pale. 

There is no icterus, clubbing, cyanosis, pedal edema, generalised lymphadenopathy on examination. 

Weight- 54 kgs

Height- 162 cms 

BMI- 20.57 kg/m2

BP- 110/70mm Hg

Hair, nails, skin and spine- normal

Systemic examination: 

Neurological examination: 

Higher mental functions: The patient is conscious, appears comfortable, language and behaviour appears normal.

Orientation to time place and person normal. Mood and emotional status appears normal.

Memory: immediate, recent and remote memory tested- normal.

Mini mental status examination score- orientation-5/5

Registration-3/3

Attention and calculation- 2/5

Recall- 3/3

Total score- 25/30

No illusions or hallucinations 

Speech: normal verbal output, fluency, repetition, naming, reading, writing.

Appearance- no tics, tremors, myoclonus, involuntary or voluntary movements 

Motor examination: 

Bulk: 

upper limb- right upper limb- 24.5 cms above elbow, 22cms below elbow

Left upper limb- 23.5cms above elbow, 22 cms below elbow

Lower limb- right lower limb- 43 cms above knee, 32 cms below knee

Left lower limb- 43 cms above knee, 32 cms below knee

Tone: hypotonic in right upper limb and lower limb, hypotonic in left upper limb and lower limb.

Power:                                       Right            Left

 Upper limb- distal flexors-       -4/5               -4/5

                      Proximal flexors 3/5                 3/5

 Hand muscles- extensor pollicis longus- 3/5 on both sides, all the others are 4/5 power

Trunk muscles- 3/5 on both sides 

Lower limb- hip muscles- iliopsoas- 3/5 on both sides

Adductor femoris- 3/5 on both sides

Hamstring muscles- 3/5 on both sides

Gastrocnemius muscles- -4/5 on both sides

Extensor hallucis longus- -4/5 on both sides

Coordination- normal coordination of movements 

Reflexes: biceps- reduced but present + on both sides

Supinator- + on both sides

Triceps- + on both sides

Ankle - + on both sides

Plantar- flexor response on both sides

Sensory examination: 

Touch- normal on both sides

Temperature- both hot and cold sensation normal on both sides

Vibration- normal on both sides

Joint position- 5/6 times on right side, 6/6 times on left side

Cerebellar examination: 

Hypotonia- present

No rebound phenomenon 

Finger nose test- normal

Finger finger test- normal

Heel shin test- normal

No past pointing, intentional tremor or gait abnormalities.

Gait: normal stride, Normal width, normal turning, the patient is not able to walk on toes.

Cranial nerves: normal smell and vision

Pupillary light reflex- normal, accommodation reflex - normal, normal manual perimetry, normal primary eye movements, normal sensations over the face, normal glabellar tap, corneal reflex, conjunctival reflex and jaw jerk, normal facial expressions, normal taste sensations all over tongue, no deviation of facial muscles or tongue muscles. Normal shrugging, head turn against pressure.

Autonomic system: no bowel bladder abnormalities, no abnormal sweating, no orthostatic hypotension, no postprandial syncopal attacks, no history of falls with loss of consciousness.

Intracranial pressure: no signs of raised intracranial pressure

Skull and spine: normal

Cardiovascular system: 

Inspection: normal on inspection, no visible pulsation, apex beat not visualised. No visible lesions on chest. Equal and symmetrical chest movements with respiration.

Palpation: apex beat felt on the left 5th intercostal space 1cm medial to mid clavicular line. All the findings of inspection are confirmed.

Percussion- all the borders of heart normal on percussion 

Auscultation- s1, s2 heard.

No added sounds, no murmurs heard, normal split heard in s2.

Respiratory system: 

Inspection- normal on inspection, no visible pulsation, apex beat not visualised. No visible lesions on chest. Equal and symmetrical chest movements with respiration.

Palpitation- apex beat felt on the left 5th intercostal space 1cm medial to mid clavicular line. All the findings of inspection are confirmed.

Percussion- no abnormal findings on percussion 

Auscultation- normal vesicular breath sounds heard equally on both sides

Abdominal examination: 

Inspection- normal on inspection, no visible pulsations, no visible lesions on abdomen.

Palpation- no organomegaly

Percussion-

Auscultation- bowel sounds heard at normal frequency 

ECG - 

                                                     

Chest X-ray- normal

                                                

Serum creatine phoshokinase- 780 IU/ lit

Nerve conduction study- normal 

Elctromyography- reduced amplitude with polyphasic motor response- suggests myopathy

Muscle biopsy report- 

                                          

Final diagnosis: Based on the above history, examination and findings, the most probable diagnosis is progressing symmetrical proximal muscular dystrophy involving both lower limbs and upper limbs without any known family history or heart involvement so most probably could be beckers or limb girdle muscular dystrophy based on the above mentioned findings.

Differential diagnosis- the other possible diagnosis could be chronic inflammatory demyelination syndrome but it is predominantly sensory and in this case sensory findings are minimal.

Other possible diagnosis could be proximal motor neuropathy or neuronopathy but there is no history of diabetes or involvement of muscles of neck, swallowing.-------------------------------------------------------------------------------------------------SHORT CASE-1:

Informant: patient’s daughter 

A 58-year-old woman presented with the complaints of 

Chief complaints: Shortness of breath with exertion since 1 year and at rest since 15 days

Cough intermittently since 4 months

Swelling of both lower limbs on and off since 2 months

Swelling of right lower limb since 10 days

History of present illness: the patient had complaint of shortness of breath since 1 year which was present with farm work started insidiously, progressing over time, exertional, non seasonal, reached the present state of shortness of breath at rest. Associated with increase during sleeping position and relieved during sitting or standing position.

Complaint of cough with expectoration intermittently, associated with worsening of chest pain, not associated with fever, no diurnal variations. Expectorant- whitish to slightly pinkish in colour, not foul smelling, no plugs, no frank blood.

Complaint of bilateral pedal edema on and off since 2 months, pitting present, extending till ankles, equal on both sides. 

Not associated with chest pain, dizziness, loss of consciousness, abnormal sensations of heart beat.

Not associated with fever, loss of weight.

Associated with increased frequency of urination since 4 months

Past history: No history of similar complaints before 1 year. History of hospitalisation for 3 times in the past one year. Episodes of hospitalisation associated with worsening of shortness of breath, pedal edema and cough. Each time the patient’s attenders gave history of on and off medication intake. 

No history of diabetes, hypertension, bronchial asthma, tuberculosis, jaundice.

No known drug allergies.

Family history: no history of similar complaints in the family. No history of sudden cardiac death in the family.

General physical examination: The patient appears conscious, cooperative, dyspnoea at rest present.

Pulse- rate 86 beats per min 

Rhythm- regular, volume- low volume, equal pulses on both sides and in all peripheral areas, no radio radial delay, no radio femoral delay.

Blood pressure- 120/60mm Hg

Jugular venous pressure- engorged vein, pulsation, the patient has hepatojugular reflex

Respiratory rate - 24 cycles per minute

Spo2 - 96% on room air

Pallor- present, no icterus, cyanosis, clubbing, lymphadenopathy. 

Pedal edema- present, bilateral pitting type, extending till ankles.

Cardiovascular examination: 

Inspection: 

No deformity or bulge in the precordium, apical impulse seen in sixth intercoastal space 1cm lateral to the midclavicular line, no diffuse pulsations over precordium, no superficial engorged veins. No scars or sinuses over the skin.

Pulsations seen on the right parasternal region and in the epigastrium.

No prominent pulsations in  the aortic, suprasternal area, supraclavicular area, no visible carotid pulsation, no visible pulsations on the back.

No kyphosis, scoliosis, drooping of shoulder, winging of scapula.

Palpation: 

Apex beat present in the 6th inter coastal space, left sided, 1cm lateral to the midclavicular line over 2 inter coastal spaces. Parasternal heave present on the right parasternal region, obliterated on pressure. 

Palpable second heart sound in the pulmonary area, not associated with palpable thrill in the pulmonary area.

No other palpable heart sounds, no thrill in carotid pulse, no superficial veins.

Percussion- right border of heart- dull ness on percussion seen till 2.5 cms lateral to the sternal border. Other borders not well localised. 

Auscultation: 

cardiac rate- about 87 beats per minute

Regular in rhythm

Mitral area- soft s1 heard, associated with diastolic murmur mid to late low pitched, no presystolic accentutation, more heard on the left lateral position. No radiation of the murmur heard.

Difficult to appreciate when the patient initially came to the hospital but better audible after initial management.

Pulmonary area- loud p2 heard, no murmur heard, no added sounds

Aortic area- s2 with normal split heard, no murmurs or added sounds heard

Tricuspid area- no murmurs or added sounds heard

Provisional diagnosis- based on the above history and examination the most probable diagnosis is moderate to severe mitral stenosis with frequent acute exacerbations of heart failure.

                                          

                                         

                                             

-------------------------------------------------------------------------------------------------

SHORT CASE-2:

Informant- patient 

Chief complaints: A 54 year old male patient came with Pain in the left side of the chest radiating to the back side since 8 days, difficulty in breathing since two days.

History of present illness: Patient was apparently asymptomatic 8 days back then he developed pain in the left side of chest all over, of stabbing type, which increased on inspiration, radiating to the left upper back.

Pain associated with difficulty in breathing with pain during inspiration, progressing over time, increased with intermittent cough.

Not associated with high grade fever, chills.

No history of shortness of breath before 8 days.

No history of palpitations orthopnoea, PND, headache, burning micturition, vomiting loose stools, cough, fever.

No history of headache, tingling sensation, numbness.

No history of decreased urine output.

History of burning sensation of both feet since 1 year, associated with tingling sensation of both lower limbs extending till ankle, equal on both sides, difficulty in feeling chappals while walking.

Past history: 

The patient has reduced vision in the right eye post trauma and also sustained a leg injury during trauma after which he started using a stick to assist his walking.

He was also operated 10 years back due to a mass in the scrotum (? Inguinal hernia)

There is no history of Hypertension, Diabetes mellitus, epilepsy, bronchial asthma, coronary artery disease.

Family history: no history of similar complaints in the family

Personal history: The patient is a chronic alcoholic and consumes about 180ml of alcohol per day, 4-5 days per week. Not a known smoker. Married and has 2 kids.

General physical examination: On Examination the patient was in sitting position, conscious coherent and cooperative.

Febrile to touch- 99.3F

Pulse- 98 beats per minute, regular, normal volume, no radio radial or radiofemoral delay 

BP 120/100mmHg

No pallor, icterus, clubbing, lymphadenopathy, pedal edema

Spine appears normal

Respiratory examination:

Upper respiratory tract: nose, septum, sinuses, oral cavity and pharyngeal cavity normal.

No mouth breathing.

Lower respiratory tract:

Inspection: The patient is sitting in proper light and was examined. Shape appears to be elliptical. Movements of chest slightly reduced on the left side of chest. Apical impulse not visible. Abdominal type of respiration. About 19 cycles per minute. No visible deviation of trachea. No visible veins or pulsations. No scars, marks or sinuses. Inter coastal fullness present on the left side localised to the lower half. No accessory muscle usage. Normal nipples and muscles on inspection. No audible sounds. No shoulder or spine abnormalities on inspection.

Palpation: Normal surface temperature. No local tenderness. No deviation of trachea. Reduced chest movement on the left side. No spinal or shoulder deformity. Asymmetrical chest expansion seen with reduced movements on the left side. Reduced vocal fremitus in the left infrascapular and left infraaxillary region.

Percussion: Stony dull note on percussion in the left infrascapular region and left infraaxillary region. Normal resonant note in all the other areas.

Auscultation: Bilateral air entry present. Equal sounds on both sides. Normal vesicular breath sounds in right infraclavicular, clavicular, supraclavicular, mammary, scapular, suprascapular, infra scapular and inter scapular regions.

Reduced breath sounds in left infrascapular region and left infra axillary region.

Reduced vocal resonance in the left sided infra axillary and infrascapular regions.

Provisional diagnosis: Based on the above history and examination, the most probable diagnosis is left sided pleural effusion, probably secondary to infection.

Investigations: total leukocyte count- 18000/cumm, hemoglobin- 14Gm/dL, platelets-2.89 lakhs/cumm

                                                

                                               

18100006009 THESIS

AUGUST 10, 2021

TITLE: 

“EVALUATION OF CAROTID INTIMAL MEDIAL THICKNESS AND ESTIMATED GLOMERULAR FILTRATION RATE IN CHRONIC KIDNEY DISEASE”

INTRODUCTION: 

Chronic kidney disease is characterized by a decrease in glomerular filtration rate and histological evidence of reduction in nephron population1. 

The clinical course is typically one of a progressive loss of nephron function leading to end stage renal disease. 

Kidney failure is the most common of the spectrum, but it represents only a minority of the total population affected by kidney disease. 

The time between initial onset of disease and development of end stage renal failure may vary widely not only between different diseases with different histopathological findings but also in different patients with similar disease processes. 

The progressive nature of CKD and the final stage ESRD is putting a substantial burden on global and national health resources since all modalities of treatment are expensive. 

There are multiple causes of kidney injury that lead to the final common pathway of end stage renal disease, and this syndrome is characterized by hypertension, anaemia, nutritional impairment, neuropathy, renal bone disease, impaired quality of life, and reduced life expectancy. 

Increasing evidence acquired in the past decades indicates that the adverse outcomes of CKD such as renal failure, cardiovascular disease, and premature death can be prevented or delayed by early detection of CKD3. 

Earlier stages of CKD can be detected through laboratory testing only. 

Treatment of earlier stages of chronic kidney disease, as well as initiation of treatment of cardiovascular and other risk factors at early stages of CKD should be effective in reducing the rate of progression of CKD to ESRD. 

In patients with CKD, the atherosclerotic cardiovascular disease is leading cause for morbidity and mortality2. 

Carotid intima-media thickness (CIMT) has been used as a marker for early atherosclerosis in patients.

 The increased incidence of CVD is the consequence of a high prevalence of both traditional risk factors, uraemia-related, and “new factors,” such as infections (Herpes virus and Chlamydia pneumoniae) and hyper-homocysteinemia, oxidative stress, which increases atherosclerotic risk among these patients. 

According to the 1999-2004 National Health and Nutrition Examination Survey (NHANES), the prevalence of Chronic Kidney Disease among the USA population is 15.3%. 

It becomes apparent that the severity of CKD along with CVD severity in any population makes a very fatal combination for both patients and healthcare systems. 

Approximately 50% of patients with ESRD die from a major cardiovascular event , which indicates a cardiovascular mortality that is 14 30times higher in dialysis patients and 500 times higher in 25- to 34- year-old ESRD patients than in individuals from the general population of the same age. 

Studies have suggested that carotid intimal medical thickness can be used as a screening test as well as marker for atherosclerosis in cardio vascular disease.

Non-invasive assessment of intima medial thickness of carotid arteries by B – mode ultrasonography is used widely in observational studies and trials as an indicational measure of generalised atherosclerosis. 

Increased intimal medial thickness of carotid arteries has been associated with disadvantageous levels of established cardiovascular risk factors, prevalent cardiovascular disease and atherosclerosis somewhere in the arterial system. 

In this study the attempt to evaluate the association of increased intimal medial thickness with traditional and non-traditional cardiovascular risk factors in CKD patients was tried. 

AIM:

Study of the carotid intimal medial thickness and estimated glomerular filtration rate in patients with Chronic Kidney Disease 

OBJECTIVES:

Determine the stage of chronic kidney disease (CKD) depending on estimated glomerular filtration rate (eGFR) 

To assess the carotid intimal medial thickness and estimated glomerular filtration rate in different stages of chronic kidney disease 

To study the effect of cardiovascular risk factors on the grade of chronic kidney disease based on history and lipid profile of the patient. 

To assess the carotid intimal medial thickness for detection of atherosclerosis in chronic kidney disease patients. 

PATIENTS AND METHODS:

PLACE OF STUDY: The patients attending Internal medicine and nephrology department in Kamineni Institute of Medical Sciences, Narketpally. 

STUDY DESIGN: Single centre, Cross sectional study 

DURATION OF STUDY: 2 years (i.e. October 2018 to September 2020). 

SAMPLE SIZE: 60 cases over 2 years 

INCLUSION CRITERIA: 

Patients diagnosed with chronic kidney disease getting treated at Department of Internal Medicine and Nephrology at Kamineni Institute of Medical Sciences, Narketpally. 

EXCLUSION CRITERIA:

Patients with Nephrotic syndrome 

Patients using statins 

Patients on treatment with antiplatelets 

Patients presenting with acute on chronic kidney disease 

Patients with previous history of cardiovascular events

CONCLUSION AND SUMMARY: 

High prevalence in traditional risk factors like diabetes, hypertension, smoking, age, alcohol, increased BMI was studied along with high prevalence in non-traditional risk factors like anaemia was studied.

More than half of the study population were illiterates 

Less than 1/10th of patients showed positive family history 

Carotid intimal medial thickness is a strong predictor of cardiovascular disease in CKD patients and maybe usefully applied in this group of patients 

Association of carotid intimal medial thickness with diabetes mellitus in CKD patients is strong and maybe useful in this group of patients 

Association of carotid intimal medial thickness with a non traditional risk factor like anaemia is strong as was correlated in this study 

Association between carotid intimal medial thickness and dyslipidemia could not be established in this study 

Association of carotiod intimal medial thickness with hypertension, smoking, alcoholism and obesity could not be correlated in this study 

Identifying modifiable risk factors for the progression of cardiovascular disease may lead to targeted medical interventions in high-risk groups.

LINK TO COMPLETE THESIS WITH MASTER CHART

https://drive.google.com/file/d/167mtL-h9yvB-K5HFSsekrEyKhxIYKjNT/view?usp=drivesdk

18100006009 LOG BOOK

AUGUST 10, 2021

I worked in kamineni institute of medical sciences as a post graduate in general medicine for 3 years. In this span I have to say that I saw the most interesting cases especially in the first half of my post graduation before covid. 

A few cases I’ve found interesting are

1. A case of 24/M who had history of red coloured urine during night came with complaints of weakness, easy fatiguability and turned out to have paroxysmal nocturnal hemoglobinuria confirmed later on flow cytometry with minimal splenic vein thrombus covering about 30% of the lumen and is on followup

2. A 22/F came with history of chronic anemia turned out to be thalassemia trait with family history

3. A 21/F came with status asthmaticus (previous history of intubation and status asthmatic is present) and status epilepticus and was intubated for 7 days and was my first case that was extubated.

4. A case of 58/M with olanzapine induced dilated cardiomyopathy on maintainance haemodialysis well maintained over a year with only 1 hospitalisation history despite dialysis and heart failure

5. A case of 32/M with prosthetic valve and infective endocarditis of mitral valve

6. A 56/M with long standing diabetes mellitus with severe autonomic dysfunction presented with severe diabetic diarrhoea about 30 episodes of stools of normal consistency which responded to ondansetron after 5 days

7. A case of 16/F unmarried woman came with recurrent vomitings, raised liver parameters and turned out to self abort herself just before she got admitted in the hospital

8. A 30/M who came with community acquired pneumonia which was minimal on radiology and on examination on the first day with severe respiratory alkalosis turned out to involve the entire inferior sub pleural region of the right lung and had severe pleural pain

9. A 15/F came with recurrent diabetic ketoacidosis with poor control and increased food intake and got intubated twice in the same year 

10. A 16/M with type 1 diabetes mellitus presented with green coloured urine, was suspected to have small intestinal bacterial overgrowth with vitamin b12 deficiency 

11. A 24/M with vitamin e deficiency induced myelopathy which reduced over 6 months with treatment and followup

12. A 35/M who was referred from psychiatry for complaining of frequent change in colour of fingers during nights, turned out to have Raynaud’s phenomenon and had interstitial lung disease on examination was found to have systemic sclerosis on followup

13. A 25/F presented with severe shortness of breath and normal chest, heart findings, with respiratory alkalosis and metabolic acidosis turned out to have an exacerbation of systemic lupus erythematosis

14. A 18/M presented with complaints of acute pancreatitis without any history of alcoholism or prominent cause and turned out to have pancreas divisum on further investigations.

15. A 63/F with history of diabetes came with unilateral involvuntary movements was diagnosed to have diabetic chorea with hyper intensities on the caudate lobe.

16. A 42/F came with history of organophosphorus poisoning is a known case of left ventricular and septal aneurysm with descending thoracic aorta aneurysm, which might be worsened if given atropine as treatment for the poisoning.

17. A 18/F with nephrotic syndrome with focal segmental glomerulosclerosis on biopsy.

18. A 60/M came with post viral severe myocarditis and pericarditis with multiple episodes of paroxysmal atrial fibrillation? Secondary to chikungunya, learnt that cardiovascular involvement in chikungunya is the second most common system involved and is frequently under diagnosed. 

Along with these few cases I’ve seen while working here, some interesting cases I’ve seen in my peripheral postings are

1. A large cardiac thrombus in the left ventricle in an asymptomatic patient

2. A case of severe pulmonary artery hypertension with multiple valvular abnormalities 

3. A diagnosed case of wegeners granulomatosis in end stage renal failure

4. A patient with bmi- 46 and metabolic syndrome on end stage renal failure

If I have to say that I learnt a procedure well, I would have to say that I developed a special interest in cardiology while working here and went to the 2d echo machine everyday in the evening with a patient and started to learn on normal hearts first. Overtime I started seeing abnormalities by myself which was overwhelming to me.

I gained a lot of experience dealing with multiple acute kidney injuries, chronic kidney disease cases with the exposure any nephrology post graduate would have normally and gained confidence in managing an emergency patient with renal failure.

I gained a lot of experience in placing central venous catheters, right jugular, left jugular and femoral catheters. I placed atleast 73 catheters during my nephrology peripheral postings. 

https://youtu.be/Ujl5QFI8hTo

HALL TICKET 18100006010

CASE PRESENTATIONS

AUGUST 10, 2021

LONG CASE: 

A 45 year old male, daily wage labourer came to the casualty with  

CHIEF COMPLAINTS:

Imbalance while walking since 3 days associated with Swaying to both the sides since 3 days. Involuntary movements of the extremities since 3 days.

HISTORY OF PRESENT ILLNESS:

Patient was apparently asymptomatic 3 days back then in the morning after he had his breakfast he noticed *imbalance while walking along with swaying on both the sides which was sudden in onset, progressive in nature, associated with generalized weakness and falls without loss of consciousness. *Involuntary movements of the extremities particularly upper limbs since 3 days, symmetrical, which was aggravating while trying to reach an object and relieving with rest, interrupting with his daily activity.

No history of buckling of limbs

No history of stiffness of limbs

No history of difficulty in getting up from squatting position

No history of any difficulty in rolling over the bed.

No history of otorrhea or any hearing loss or any earache.

No history of giddiness or lightheadedness or palpitations, dry skin

No history suggestive of wash basin attack

No history of difficulty in wearing slippers or any slippage of chappals.

No history of any root pain or paresthesias or numbness

No history of neck pain or neck stiffness or blurring of vision or projectile vomitings.

No history of urinary incontinence or retention or diarrhea or constipation.

No history of any speech abnormality or anything suggestive of  cranial nerve abnormality.

No history of fever or headache

No history of waxing or wanning of symptoms.

No history of any behavioural changes 

No history of weight loss or loss of appetite.

No history of intake of toxins.

No history of joint pains or rash

No history of bulky stools or loose stools.

PAST HISTORY:

Known case of epilepsy and on medication since 8 yrs (Tab PHENYTOIN 100MG/TID)

Not a known case of diabetes or hypertension or thyroid problems or tuberculosis.

No history of any serious illness in the past or any hospital admission 

No history of similar complaints in the past.

DRUG HISTORY:

History of excessive intake of phenytoin in the past 20 days for the fear of precipitating  seizures.

PERSONAL HISTORY:

Regular diet

Regular bowel and bladder

Disturbed sleep since past 1 month (due to anxiety and depression probably due to loss of 

his brother) Occasionally Alcoholic. Occasional Smoker: smokes 1 pack (20 cigarretes) in a week ,0.5 pack years

FAMILY HISTORY:

Born on non consanguinous marraige.

achieved appropriate developmental milestones.

No history of similar complaints in the family.

SUMMARY:

Case of a 45 Year old male with symmetrical bilateral Ataxia, sudden in onset,

I would like to consider the possibility of Acute cerebellar Ataxia without the involvement 

of  sensory, motor, autonomic or cranial nerve involvement.

GENERAL EXAMINATION:

Patient is conscious, coherent and cooperative, comfortably lying on bed. 

Well built, moderately nourished, BMI of 22kg/m2.

No pallor/ icterus /cyanosis/clubbing/ kylonychia /lymphadenopathy/edema

Hypertrophy of the gums present.

No signs of Neurocutaneous markers or any skin rash

No hyperpigmentation of knuckles.

No signs of nutritional deficiency like cheilitis or angula stomatitis or purpura or thinning of hair or dermatitis or bruising.

No spine abnormalities

No signs of skeletal deformities like pes cavus , short neck.

No detectable KF rings or sunflower cataract or telangiectasias.

VITALS:

PULSE: regular rhythm

               82 BPM

               good volume

               normal character

               normal vessel wall thickening

               no radioradial or radiofemoral delay.

               peripheral pulses felt.

BLOOD PRESSURE: right arm supine position.

                                     132/90mm of hg

RESPIRATORY RATE: 22CPM, regular, abdominothoracic type.

TEMPERATURE         : afebrile

SYSTEMIC EXAMINATION:

CNS:

Right Handed person, studied upto 10th standard.

HIGHER MENTAL FUNCTIONS:

Conscious, oriented to time place and person.

MMSE 26/30

speech: normal

Behavior: normal 

Memory: Intact.

Intelligence: Normal

Lobar Functions: Normal.

No hallucinations or delusions.

CRANIAL NERVE EXAMINATION:

1st  : Normal

2nd  :  visual acuity is normal

           visual field is normal

            colour vision normal

            fundal glow present.

3rd,4th,6th  :  pupillary reflexes present.

                      EOM full range of motion present

                      gaze evoked Nystagmus present.

5th             :  sensory intact

                      motor intact

7th             :  normal

8th             :  No abnormality noted.

9th,10th     : palatal movements present and equal.

11th,12th   : normal.

MOTOR EXAMINATION:                     Right                                           Left

                                           UL                            LL                      UL                    LL

   BULK                         Normal                    Normal                 Normal          Normal

   TONE                          hypotonia                hypotonia             hypotonia      hypotonia

   POWER                       5/5                          5/5                         5/5                 5/5

   SUPERFICIAL REFLEXES:

   CORNEAL                                    present                                            present       

   CONJUNCTIVAL                         present                                            present

   ABDOMINAL                                                             present

   PLANTAR                                     withdrawal                                      withdrawal

   DEEP TENDON REFLEXES:

   BICEPS                        2                                2                         2                       2

   TRICEPS                      2                                2                         2                       2

   SUPINATOR                2                                2                         2                       2

   KNEE                            2                               2                         2                       2

   ANKLE                         1                               1                         1                        1

SENSORY EXAMINATION:  

SPINOTHALAMIC SENSATION:

Crude touch

Pain

Temperature

DORSAL COLUMN SENSATION:

Fine touch

Vibration

Proprioception

CORTICAL SENSATION:

Two point discrimination

Tactile localisation.

Steregnosis

Graphasthesia.

CEREBELLAR EXAMINATION:

  Finger nose test

  Heel knee test 

  Dysdiadochokinesia

  Dysmetria

  Hypotonia with pendular knee jerk present.

 Intention tremor present.

  Rebound phenomenon.

  Nystagmus

  Titubation

  Speech

  Rhombergs  test

SIGNS OF MENINGEAL IRRITATION: absent

GAIT:

Wide based with reeling while walking, unsteady with a tendency to fall

unable to perform tandem walking.

CVS EXAMINATION:

   S1 S2 Present

  No murmurs or added sounds

RESPIRATORY SYSTEM EXAMINATION:

  Bilateral airway entry

  No added sounds.

PER ABDOMEN EXAMINATION:

  Soft and nontender.

  No organomegaly present.

FINAL DIAGNOSIS:

FUNCTIONAL:       ATAXIA

ANATOMICAL:      CEREBELLUM

PATHOLOGICAL:

ETIOLOGICAL:     ? DRUG INDUCED(PHENYTOIN)

WORKUP:

CBP:

        HB  11.2

        TLC  12000

      PLATELET  2.02L

ESR    23

LFT    Within normal limit

RFT    Within normal limit

ECG   

                    

CXRAY

-------------------------------------------------------------------------------------------------

SHORT CASE-1:

A 60 years old female presented to the casualty with complaints of fever associated with chills and abdominal pain.

CHIEF COMPLAINTs

➤Fever for the past 6 days.

➤Pain abdomen for the past 3 days

HISTORY OF PRESENTING ILLNESS

Patient was apparently asymptomatic 6 days ago after which she developed high grade fever associated with chills, insidious in onset, progressive, not subsiding with medication, continuous type

Pain abdomen, sudden in onset, pricking type, in the epigastrium and right hypochondrium which gets aggravated on right lateral position and relieved with sitting posture, associated with nausea and reduced appetite, no association with intake of fatty food

No complaints of burning micturition.

No complaints of cough, cold or shortness of breath.

No complaints of heartburn or flatulence.

No complaints of heamatemesis or maleana.

No complaints of dysphagia.

No complaints of constipation or diarrhoea.

No history of yellowish discolouration of eyes or high coloured urine.

No history of weight loss

No history of any blood transfusion

No history of any high risk behaviour

HISTORY OF PAST ILLNESS 

   Not a known case of hypertension, diabetes, bronchial asthma, epilepsy.

   k/c/o tuberculosis and took complete treatment.

   No history of similar complaints in the past.

DRUG HISTORY

➤No significant drug history or intake of toxins.

PERSONAL HISTORY

➤Occupation: Daily waged labor working in Cotton fields.

➤Patient is married

➤Patient takes mixed diet but has a decreased appetite.

➤Bowel and bladder movement is normal and regular.

➤occasional Alcoholic, non smoker.

- sound sleep

FAMILY HISTORY 

➤No significant family history.

MENSTRUAL HISTORY:

G 3 P 4 L 4 A 0

Attained menarche at the age of 20 years, with good flow and volume.

Attained menopause at age of 42 years.

SUMMARY:

60 year old female with high grade fever and  abdominal pain confined to

 right upper quadrant, acute in onset, without any alcohol history.

Possibly case of 

1) Acute Liver injury (?infective etiology)

2)Acute Cholecystitis.

GENERAL EXAMINATION 

Patient is well built, well nourished.

➤Pallor: Not seen

➤Icterus:  Not seen

➤Cyanosis:  Not seen

➤Clubbing:  Not seen

➤Lymphadenopathy:  Not seen

➤Edema:  Not seen

- No signs of chronic liver cell failure

- No signs of nutritional deficiency.

VITALS

➤Temperature: 101℉

➤PR: 108 beats per minute

➤BP: 100/70 mmHg

➤RR: 24 cycles per minute

➤SpO2: 95% in room air

➤Blood Sugar (random): 100mg/dl

SYSTEMIC EXAMINATION 

ABDOMINAL EXAMINATION

INSPECTION

➤Shape - Scaphoid, with no distention.

➤Umbilicus - Inverted

➤Equal symmetrical movements in all the quadrants with respiration.

➤No visible pulsation,peristalsis, dilated veins and localized swellings.

PALPATION

➤SUPERICIAL: Local rise of temperature in right hypochondrium with tenderness

 and localised guarding and rigidity.

➤ DEEP: Mild enlargement of liver, regular smooth surface, rounded

 edges soft in consistency, tender, moving with

 respiration non pulsatile

➤No splenomegaly

➤Abdominal girth: 78cms.

➤xiphesternum to umbilicus distance was equal to umbilicus to pubic distance.

PERCUSSION

➤Hepatomegaly:  liver span of 16 cms with 4 cms extending

 below the costal margin

➤Fluid thrill and shifting dullness absent 

➤Puddle sign absent

➤Traubes space: resonant

 AUSCULTATION

➤ Bowel sounds present.

➤No bruit or venous hum.

NO LOCAL LYMPHADENOPATHY

PER VAGINAL AND PER RECTAL EXAMINATION: NAD 

CARDIOVASCULAR SYSTEM EXAMINATION

➤s1 and s2 heard

➤Thrills absent.,

➤No cardiac   murmurs

RESPIRATORY SYSTEM

➤Normal vesicular breath sounds heard.

 ➤Bilateral air entry present

CENTRAL NERVOUS SYSTEM EXAMINATION

➤Conscious and coherent

PROVISIONAL DIAGNOSIS:  

ACUTE HEPATITIS (? INFECTIVE)

INVESTIGATIONS: 

DAY 1

Serum Na+ 126

Serum K+    4.7

Serum Cl-    92

Serum Creatinine 0.8

Blood urea             40

CUE             normal

CBP:  HB 10.7

           TLC  13900

           PLATELET 4.02L

LFT:   TB        2.45

            DB       1.59

            SGOT  52

            SGPT  10

            ALK P  191

            ALB      2.5

PT/INR             17/1.2

APTT                33SECS

ESR                  110

BLOOD CULTURES    Showed no growth.

                                               USG ABDOMEN

       

USG REPORT IMPRESSION-

Multiple liver abscess with largest measuring 5*5 cms in the 7th segment of liver , with 40 to 50% of liquefaction , hepatomegaly with liver span of 18.5 cms.

CT SCAN

XRAY CHEST-POST TB CHANGES

FINAL DIAGNOSIS :

MULTPLE  PYOGENIC LIVER ABSCESS WITH ACUTE LIVER FAILURE.

TPR CHART

-------------------------------------------------------------------------------------------------

SHORT CASE-2:

A 48 yr old male, farmer by occupation & resident of Nakrekal came to casualty with

CHEIF COMPLAINTS:

1.Swelling in the right lower limb since 20 years

   associated with pain 

2.Fever since 1wk

3.Loose stools  since 4 days (4 episodes/day)

HISTORY OF PRESENT ILLNESS :

Patient was apparently asymptomatic 20years back then, he developed

1) SWELLING IN THE RIGHT LOWER LIMB:

 -Patient is a known case of filariasis with right leg swelling since 20 years which gets aggravated with rest and subsided with walking intermittently also associated with fever spikes which gets relieved with medication

- Patient had a trauma over right lower limb 4 days back, following which patient noticed increased swelling over right leg with ulceration and pus discharge associated with pain of pricking type.

 2) FEVER:

- Low grade, intermittent type, associated with chills & rigors, since 1 week & relieved by medications.

- He got admitted for the same in a nearby hospital and was told that

  his platelet count is low for which he was receiving conservative   

  treatment, as he could'nt afford the charges so was shifted here.

3)LOOSE MOTIONS:

-Patient had loose motions since 4 days, upto 4 episodes per day,

  not blood stained, non mucoid, low volume, non foul smelling. 

 No history of body pains, abdominal pain, headache.

 No history of nausea ,vomitings or diarrheoa.

 No history of oliguria or burning micturition.

PAST HISTORY: 

- No similar complaints in the past

-Not a k/c/o DM, HTN, Asthma, TB, Epilepsy.

-No history of any drug usage or intake of toxins.

FAMILY HISTORY - 

-No significant family history 

PERSONAL HISTORY- 

- Diet              :mixed

- Appetite       :normal

- Sleep            : adequate 

- Bladder        : regular.

- Bowel          : diarrheoa since 4 days.

- Addictions   : Absent 

GENERAL EXAMINATION:

Patient is conscious, coherent, cooperative. 

well built, moderately nourished.

- No pallor 

- No icterus 

- No clubbing, cyanosis 

- No koilonychia

- No lymphadenopathy

- No Edema 

- No rashes, Petechiae & Bleeding manifestations 

-Tourniquet test - Negative 

VITALS:

1.Temperature: Afebrile 

2. BP               : 100/70mmHg

3. PR               : 74 bpm

4. RR              :  24cpm.

SYSTEMIC EXAMINATION:

PER ABDOMEN:

- No distended abdomen

- No abdominal tenderness

- No engorged veins

- Guarding & rigidity absent

- Bowel sounds present.

RESPIRATORY SYSTEM:

-Bilateral airway entry present

-No added sounds

CVS:

- S1S2 Heard

- No thrills no murmurs

CNS:

-No abnormality noted

- Higher mental functions intact.

LOCAL EXAMINATION:

PROVISIONAL DIAGNOSIS:

-ELEPHENTIASIS WITH CHRONIC LYMPHEDEMA

-DENGUE FEVER

 FEVER CHARTING:

SURGERY REFERRAL:

INVESTIGATIONS:

HEMOGRAM:

DATE: 4/08/21

- TOTAL WBC COUNT - 5,250 cells/cumm (N - 4,000 to 10,000 cells/cumm)

- PLATELET COUNT - 1.99 lakhs/cumm (N - 1.5 - 4.1 lakh/cumm)

- PCV - 38.3% (N - 40 - 50 %)

- 6/08/21

- TOTAL WBC COUNT - 3,500 cells/cumm 

- PLATELET COUNT - 1.25 lakhs/cumm

- PCV - 46%

- 7/08/21

TOTAL WBC COUNT - 2,150 cells/cumm 

- PLATELET COUNT - 44,000 cells/cumm 

- PCV - 39%

- 8/08/21 (MORNING)

- TOTAL WBC COUNT - 3,650 cells/cumm 

- PLATELET COUNT - 39,000 cells/cumm 

- PCV - 39.4%

- 8/08/21 (EVENING)

- TOTAL WBC COUNT - 4,200 cells/cumm 

- PLATELET COUNT - 60,000 lakhs/cumm 

- PCV - 39.1%

- 9/08/21 (Morning)

Evening 

DENGUE RAPID TEST 

MALARIAL PARASITE TEST 

LFT

CUE

RBS

BLOOD UREA 

SERUM CREATININE 

SERUM ELECTROLYTES 

ECG 

TREATMENT 

DATE - 08/08/21

1. IVF @ 75 Ml/hr 

- 1. NS

- 1. RL

- 1. DNS

2. TAB PCM 650 MG X PO X TID

               1 - 1 - 1

Check temperature before giving pcm 

3. TEMPERATURE CHARTING 4TH HRLY

4. GRBS CHARTING 6TH HRLY

5. I/O CHARTING 

DATE - 9/09/21

1. IVF @ 75 Ml/hr 

- 1. NS

- 1. RL

- 1. DNS

2. TAB PCM 650 MG X PO X TID

               1 - 1 - 1

3. TAB AUGMENTIN 625 MG X OD X BD

4. TAB PAN 40 MG X OD

5. TAB MVT ORAL OD

6. TAB VIT C ORAL OD

7. TAB DOLO 650 MG ORAL (SOS)

8. Check temperature before giving pcm 

9. TEMPERATURE CHARTING 4TH HRLY

10.GRBS CHARTING 6TH HRLY

11. I/O CHARTING 

18100006010 THESIS

AUGUST 10, 2021

TITLE:

SIGNIFICANCE OF SERUM PSEUDOCHOLINESTERASE LEVELS IN PATIENTS WITH ORGANOPHOSPHORUS COMPOUND POISONING”

INTRODUCTION:

Acute poisoning is important cause of morbidity and mortality in India. In medical emergency 10% of admissions are due to poisoning and organophosphorus poisoning contributes to nearly 50% of it.[1] Apart from use of these substances as agricultural insecticides, pesticides, they are frequently abused for suicidal purposes because of their low cost, rapid action and easy availability. They have been imported in India since 1951, but very few knew the nature of these compounds as a virulent poison till the Kerala food poisoning tragedy in 1958. This tragedy took a toll of hundred and add due to inadvertent stocking of food stuff and folidol packages in the same hold where the folidol containers leaked and contaminated the gunny bags containing food stuff [2]. Exposure to organophosphorus compounds in the form of nerve agents and pesticides poses an ever increasing military and civilian threat [3] the majority of patients are younger than 30 yrs. [5] In teenagers and adults the poisoning is generally due to suicidal intention though accidental poisoning occurs during spraying [2] They act by irreversibly inhibiting the enzyme cholinesterase resulting in accumulation of acetylcholine at synapses and myoneural junction and leads to cholinergic over activity.[6][7][8]

AIMS AND OBJECTIVES

AIM:

 To study the significance of serum pseudocholinesterase levels in patients with organophosphorus compound poisoning.

OBJECTIVES:

 To study the clinical manifestations in patients with organophosphorus compound poisoning

 To study the prognostic and diagnostic value of serum pseudocholinesterase levels in patients with organophosphorus compound poisoning.

 To study the outcome of patients with organophosphorus compound poisoning.

MATERIALS AND METHODS:

SOURCE DATA:

This study was undertaken from October 2018 to September 2020 at Kamineni Institute of Medical Sciences, Narketpally.100 patients of suspected organophosphorous poisoning admitted to medical emergency ward, Kamineni Institute of Medical Sciences have formed the material for the study.

STUDY DESIGN:

Single centre

Prospective study

INCLUSION CRITERIA:

In this study patients above 18 years with suspected Organophosphorus compound poisoning

EXCLUSION CRITERIA:

• OP compound poisoning cases < 18 years of age.

• H/o consumption of other drugs along with OP compound

• H/o preexisting hepatic dysfunction which reduce the level of Pseudocholinesterase.

• History of Carbamate poisoning.

DIAGNOSIS:

Based on

1) History or evidence of exposure to organophosphorus compound within 24hours.

2) Characteristic manifestations of OPC poisoning including, miosis,

fasciculations, excessive salivation.

3) Improvement of signs and symptoms with administration of atropine.

4) Corroborative evidence like empty containers and odour of gastric aspirates.

Depending on the severity of manifestations patients were classified into three grades as mild, moderate and severe depending on serum pseudocholinesterase levels.

INVESTIGATIONS:

Soon after admission blood samples were collected and investigated to know the serum levels of pseudocholinesterase on Day 1, Day 3, and before discharge. Other routine investigations such as

• Hemoglobin percentage

• Total blood count

• Differential count

• ESR

• Random blood sugar

• Serum creatinine

were done to exclude chronic conditions.

METHOD OF ESTIMATION OF PSEUDOCHOLINESTERASE:

Method with S-butyryl thiocholine iodide using Dibucaine as inhibitor.

LINK TO COMPLETE THESIS WITH MASTER CHART:

https://drive.google.com/file/d/16rjVcmfuzhZLCYfbQYSUMUlSgAbupvKt/view?usp=drivesdk

18100006010 LOG BOOK

AUGUST 10, 2021

I feel very fortunate for practicing the branch of my choice where I get to see vast variety of cases  on day-to-day basis. Here I will be sharing few of my experiences during my junior residency. 

I have seen closely majority of cases during my first year of residency. One of the mind blowing case was of Non Hodgkins Lymphoma:

Patient presented with fever of high grade with anorexia, he was almost worked up for 2 weeks but we couldnt find any conclusive diagnosis. we ultimately labelled him as pyrexia of unknown origin. Then gradually after weeks of stay in hospital patient started developing vague abdominal pain which made us repeat his USG abdomen and Erect X ray abdomen which showed mediastinal lymphadenopathy. 

we tried palpating the rest group of lymph nodes for any enlargement but there was only mediastinal lymphadenopathy, as we couldn't get any cause for his lymph node enlargement, we planned for a lymph node biopsy CT guided, which showed features suggestive of non Hodgkins lymphoma.  

https://youtu.be/q0NvLmVuANA