THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[7:55 pm, 18/10/2025] PPM 6: C/o pain abdomen 4 days
C/o Shortness of beath x 3 days
C/o altered sensation since yesterday night
Patient was apparently normal 4 days ago, then be developed pain abdomen (right iliac region), non radiating, no aggravating factors, relieved after medication. H/o shortness of breath,
initially grade II MMRC progressed to grade IV.
H/O 2-3 episodes of vomiting since 4 days, resolved on medication, non bilious, non blood tinged, containing food particles. H/O decreased urine output 4 days ago, resolved after treatment. Patient was initially taken to a local hospital, where he was admitted and managed conservatively. H/o 3 episodes of loose stools, 2 days ago, resolved now.
HISTORY OF PAST ILLNESS No Hlo chest pain, cough, burning micturition, seizures fever
K/c/o type 2 DM since 3 years,on
Inj MIXTARD 10U--0--10U
H/o pleural effusion s/p pleural tapping done in 2014
H/o 1.SDP transfused on 16/10/25 and 4.FFPS transfused on 15/10/25
H/o Inj. Meropenem 1gm IV/BD given outside at 9:30pm (Yesterday)
[7:58 pm, 18/10/2025] PPM 1: Why was he on injection insulin since 3 years inspite of his diagnosis of type 2?
[8:02 pm, 18/10/2025] PPM 6: Only since 1 year he is using insulin as his sugars were not under control sir
[8:47 pm, 18/10/2025] PPM 1: What was he using before that?
[9:29 pm, 18/10/2025] PPM 6: Sir he is using mixtard + Glimepiride 1gm+Metformin 850mg bd
[9:30 pm, 18/10/2025] PPM 4: Glimistar sir
[9:30 pm, 18/10/2025] PPM 5: Before only on Glimepiride1gm+ Metformin 85omg bd sir
[9:33 pm, 18/10/2025] PPM 1: What is the possible reason for his ketoacidosis this time on type 2 diabetes? @PPM3 why does DKA patients often have associated pancreatitis?
@PPM4 what is the current evidence for his acute pancreatitis?
[9:43 pm, 18/10/2025] PPM 4: Outside reports serum lipase and amylase were elevated
Previously he was admitted in an outside hospital in miryalguda sir
When he came to our hospital the lipase and amylase were not elevated as such and USG abdomen pancreas is normal CT was not done sir but he has acute pain abdomen plus chronic alcoholic since 20 yrs
[9:46 pm, 18/10/2025] PPM 1: @Meta AI what is the connection between diabetic ketoacidosis and pancreatitis?
[9:46 pm, 18/10/2025] Meta AI: Diabetic ketoacidosis (DKA) and pancreatitis have a complex, bidirectional relationship. Uncontrolled DKA can increase the risk of developing pancreatitis due to metabolic disturbances and stress on the pancreas. Conversely, pancreatitis can disrupt insulin production and glucose regulation, potentially triggering DKA.¹
Shared Risk Factors:
- Hypertriglyceridemia: Elevated triglyceride levels can contribute to both conditions.
- Insulin Deficiency: Inadequate insulin can lead to DKA and worsen pancreatitis.
- Metabolic Imbalance: DKA's metabolic acidosis can stress the pancreas, increasing pancreatitis risk.² ³
Key Connections:
- Inflammation and Oxidative Stress: Pancreatitis can cause inflammation, which may contribute to DKA development.
- Insulin Resistance: Pancreatitis can lead to insulin resistance, exacerbating DKA.
Management Strategies:
- Fluid Resuscitation: Replenish fluids to prevent dehydration.
- Insulin Therapy: Regulate blood sugar levels.
- Pain Management: Control pain and discomfort.
- Monitoring: Closely track vital signs, laboratory parameters, and complications.
[9:58 pm, 18/10/2025] PPM 3: Of course. This is a complex and critical case. Based on the provided history, here is a breakdown of the possible reasons for the patient's conditions, addressing each of your questions.
### 1. What is the possible reason for his ketoacidosis this time on type 2 diabetes?
The most likely and significant reason for this episode of Diabetic Ketoacidosis (DKA) in a known Type 2 Diabetic patient is *an acute underlying illness acting as a severe physiological stressor*.
In Type 2 Diabetes, the body still produces insulin, but it is insufficient to meet the increased demands during stress. Here's the breakdown:
* *The Precipitating Factor:* The patient's symptoms started with *abdominal pain*. This acute illness (highly suspected to be pancreatitis, as discussed below) creates a massive stress response in the body.
* *The Hormonal Cascade:* Stress hormones like *cortisol, adrenaline, and glucagon* are released in high amounts.
* These hormones work against insulin (they are "counter-regulatory hormones").
* They promote severe *insulin resistance*, making the patient's existing insulin (both endogenous and the injected Mixtard) much less effective.
* They trigger the liver to produce excessive glucose (gluconeogenesis and glycogenolysis).
* *The Path to DKA:*
1. *Relative Insulin Deficiency:* The existing insulin becomes inadequate due to the severe insulin resistance.
2. *Hyperglycemia:* Blood sugar rises dramatically because glucose production outstrips its utilization.
3. *Ketogenesis:* With no effective insulin to allow glucose into cells, the body switches to breaking down fats for energy, producing acidic ketone bodies as a byproduct.
4. *Acidosis:* The buildup of ketones overwhelms the body's buffering systems, leading to metabolic acidosis (DKA).
*Other contributing factors specific to this case:*
* *Inadequate Insulin Regimen:* The patient was on a *fixed-dose, premixed insulin (Mixtard)*. This regimen is often inflexible and may not be sufficient to cover the dramatically increased insulin requirements during an acute illness. A basal-bolus regimen is typically more effective for preventing DKA.
* *Possible Pre-renal Azotemia:* The history of "decreased urine output" suggests dehydration, which worsens hyperglycemia and accelerates the progression to DKA.
*In summary: The acute abdominal illness (likely pancreatitis) acted as the powerful trigger that pushed a relatively stable Type 2 diabetic into a state of severe insulin resistance and relative insulin deficiency, culminating in DKA.*
---
### 2. Why does DKA patients often have associated pancreatitis?
The relationship between DKA and pancreatitis is complex and bidirectional. It's often a "chicken-or-egg" scenario, but in this case, the abdominal pain came first, suggesting pancreatitis may have been the trigger.
*How DKA can CAUSE Pancreatitis:*
1. *Hypertriglyceridemia:* This is the *most common cause of pancreatitis in DKA*. DKA causes a massive release of free fatty acids from fat breakdown (lipolysis). The liver responds by producing very low-density lipoproteins (VLDL), leading to severely elevated triglycerides. When triglyceride levels exceed a critical threshold (often >1000 mg/dL), they are thought to cause pancreatitis by breaking down into toxic free fatty acids that directly injure pancreatic acinar cells.
2. *Pancreatic Ischemia:* The severe dehydration and hypoperfusion in DKA can reduce blood flow to the pancreas, causing ischemic injury.
3. *Microvascular Injury:* Hyperviscosity from dehydration and hyperglycemia can damage small blood vessels in the pancreas.
*How Pancreatitis can CAUSE DKA:*
1. *Severe Physiologic Stress:* Acute pancreatitis is a major inflammatory and painful condition. As described above, this stress triggers the counter-regulatory hormone surge, leading to insulin resistance and hyperglycemia.
2. *Direct Beta-Cell Dysfunction:* The intense inflammation can have a temporary toxic effect on pancreatic islet cells, impairing both insulin and glucagon secretion, though the insulin deficiency is more clinically significant in a diabetic.
3. *Nausea/Vomiting:* This leads to dehydration and inability to take oral diabetes medications or food, disrupting glucose management.
*In this patient:* Given that abdominal pain was the very first symptom, it is highly plausible that an episode of acute pancreatitis (possibly triggered by his underlying metabolic profile) began first, and then acted as the severe stressor that precipitated the DKA.
---
### 3. What is the current evidence for his acute pancreatitis?
While a definitive diagnosis requires specific imaging and lab tests, the clinical evidence in this case is highly suggestive of acute pancreatitis.
*Supporting Evidence from the History:*
1. *The Primary Symptom: Abdominal Pain:* The very first symptom was abdominal pain. While its location in the *right iliac region* is atypical (classic pancreatitis is epigastric), pancreatitis, especially if the head of the pancreas is inflamed, can present with right-sided pain. Atypical presentations are common.
2. *Associated Gastrointestinal Symptoms:*
* *Vomiting:* Multiple episodes of vomiting containing food particles is a very common feature of pancreatitis.
* *Loose Stools:* Can occur due to the systemic inflammatory response or associated ileus.
3. *The Precipitant for DKA:* As established, a severe stressor like pancreatitis is a classic and common trigger for DKA.
4. *Historical Risk Factors:*
* *Type 2 Diabetes:* Diabetics, especially those with poor control, are at higher risk for hypertriglyceridemia, which is a major cause of pancreatitis.
* *Potential Hypertriglyceridemia:* While not confirmed with a lab value here, the presence of DKA makes severe hypertriglyceridemia a very likely underlying cause for both conditions.
*Evidence that is Currently Missing (Needs to be Checked):*
To confirm the diagnosis, the following should be pursued urgently:
* *Serum Lipase/Amylase:* A level *>3 times the upper limit of normal* is the key diagnostic criterion.
* *Abdominal Imaging:* A *Contrast-Enhanced CT (CECT) abdomen* is the gold standard to confirm pancreatitis, assess its severity, and identify complications like necrosis or fluid collections. A bedside ultrasound can be done first to look for gallstones and assess the pancreas.
* *Serum Triglyceride Level:* This is crucial. A level >1000 mg/dL would strongly point to hypertriglyceridemia-induced pancreatitis.
* *Other Labs:* *Elevated C-reactive Protein (CRP)* after 48 hours indicates severity. *Hypocalcemia* is a poor prognostic sign. *Leukocytosis* is common.
*Conclusion on Acute Pancreatitis:*
The clinical picture is *highly consistent with acute pancreatitis as the inciting event*. The abdominal pain preceding respiratory and neurological symptoms, combined with vomiting and the subsequent development of DKA, forms a classic narrative. The administration of Meropenem (a broad-spectrum antibiotic) at the outside hospital also suggests they were concerned for a severe intra-abdominal infection/inflammatory process.
*Immediate Next Steps:*
1. *Confirm Pancreatitis:* Check Lipase/Amylase and arrange for a CECT abdomen.
2. *Identify the Cause of Pancreatitis:* Check a fasting lipid profile.
3. *Manage the DKA Aggressively:* Continue with IV fluids, insulin drip, and electrolyte correction.
4. *Manage Pancreatitis:* Provide NPO (nil by mouth), aggressive IV hydration, and pain control.
This patient is critically ill with two life-threatening conditions (DKA and suspected severe pancreatitis) that are fueling each other, requiring intensive management.
*
*Disclaimer:* This analysis is based on the information provided and is for educational purposes. All clinical decisions must be made by the treating healthcare team based on a full physical examination and review of all laboratory and imaging results.
[22-10-2025 15.49] PPM 1: 
[22-10-2025 16.12] PPM 1: @PPM3 his current illness with vomiting and pain abdomen clinically diagnosed DKA began after the development of these bullous lesions few days back. Any differentials from your LLMs computer vision?
Here are the key differentials, ordered from most to least likely in this specific clinical context:
### Primary Differential Diagnosis (Most Likely)
**1. Bullosis Diabeticorum (Diabetic Bullae)**
* **Rationale:** This is the most direct and likely diagnosis. It is a rare but well-known condition characterized by the spontaneous appearance of tense, fluid-filled blisters in individuals with diabetes, often precipitated by periods of poor metabolic control, which is exactly what happens in DKA.
* **Clinical Clues:** The blisters are typically non-inflammatory, painless, and appear abruptly on acral areas (feet, hands, lower legs). The timing (appearing just before the systemic metabolic decompensation) is highly suggestive. It's a diagnosis of exclusion.
### Important Infectious Differentials
**2. Necrotizing Fasciitis ("Flesh-Eating Bacteria")**
* **Rationale:** This is a **critical "can't-miss" diagnosis**. Diabetic patients are profoundly immunocompromised and highly susceptible to severe soft tissue infections. The vomiting and abdominal pain could be part of a systemic inflammatory response syndrome (SIRS) or sepsis from the infection, which could also precipitate DKA.
* **Clinical Clues:** The bullae may be hemorrhagic or violaceous. The skin would be extremely tender, painful out of proportion to exam, and the patient may appear toxic and septic. This is a surgical emergency.
**3. Bullous Cellulitis / Streptococcal or Staphylococcal Infection**
* **Rationale:** Similar to above, but less rapidly progressive than necrotizing fasciitis. Common skin bacteria can cause cellulitis that forms bullae due to severe edema and toxin production.
* **Clinical Clues:** The area would be warm, erythematous, swollen, and painful. The patient would likely have fever and leukocytosis.
**4. Cutaneous Candidiasis or Mucormycosis**
* **Rationale:** Uncontrolled diabetes and DKA create an ideal environment for fungal infections. While candidiasis more commonly presents with satellite pustules, it can be bullous. Mucormycosis is a life-threatening angioinvasive fungus that can present with black, necrotic eschar, but bullous lesions can also occur.
* **Clinical Clues:** Requires a high index of suspicion, especially in the immunocompromised host.
### Autoimmune Bullous Diseases (Less Likely, but Possible)
**5. Bullous Pemphigoid**
* **Rationale:** This is an autoimmune blistering disease that has a known, though weak, association with diabetes. It can be triggered by systemic stress or illness.
* **Clinical Clues:** Blisters are typically large, tense, and appear on erythematous or normal skin, often with a generalized distribution (trunk, flexures) rather than just acral. It is usually very pruritic.
**6. Pemphigus Vulgaris**
* **Rationale:** Another autoimmune blistering disease. Less common than bullous pemphoid and usually more severe.
* **Clinical Clues:** Blisters are flaccid, fragile, and easily rupture, leaving painful erosions. Often starts in the oral mucosa.
### Other Considerations
**7. Porphyria Cutanea Tarda (PCT)**
* **Rationale:** PCT can be associated with diabetes and presents with fragile skin and bullae on sun-exposed areas (hands, arms).
* **Clinical Clues:** Skin is fragile, with milia and hyperpigmentation. The absence of a history of sun exposure and the acute onset make this less likely.
**8. Drug Eruption**
* **Rationale:** The patient may have been started on a new medication for a nascent infection or other issue, which could cause a bullous drug eruption.
* **Clinical Clues:** Requires a careful medication history. Often accompanied by a rash.
---
### Summary and Recommended Steps from a Clinical AI Perspective:
Given the history, the most probable scenario is that the **bullous lesions are a cutaneous manifestation of the underlying severe metabolic dysregulation, making Bullosis Diabeticorum the top differential.**
However, the **paramount task is to rule out a life-threatening infection like Necrotizing Fasciitis**, as the systemic symptoms (vomiting, abdominal pain) could be from sepsis rather than DKA alone, or the infection could have been the precipitating factor for the DKA.
**Key actions for the clinical team would be:**
1. **Urgent Surgical Consult:** To evaluate for necrotizing soft tissue infection.
2. **Wound Culture & Sensitivity:** Aspirate fluid from a bulla or biopsy the edge for Gram stain, culture (bacterial and fungal).
3. **Skin Biopsy:** For routine histopathology (to confirm blister level) and direct immunofluorescence (to rule out autoimmune bullous diseases). A biopsy for frozen section can be done urgently to look for "ghost cells" and fascia necrosis in suspected necrotizing fasciitis.
4. **Aggressive Management of DKA:** This is the cornerstone, as correcting the metabolic acidosis and hyperglycemia is critical for patient survival and immune function.
In conclusion, while the LLM's "computer vision" differentials point strongly to **Bullosis Diabeticorum**, the clinical imperative is to act as if it is **Necrotizing Fasciitis** until proven otherwise.
***
**Disclaimer:** This analysis is based on a textual description of a medical case and is for educational purposes only. It is not a substitute for professional medical judgment, diagnosis, or treatment. The managing physician must make all final decisions based on a full clinical evaluation.
[22-10-2025 16.30] PPM 1: 20/10/2025
22/10/2025
[4:32 pm, 22/10/2025] PPM 1: 👆Deep seek?
Which LLM's in our regular usage have computer vision @Meta AI
[4:32 pm, 22/10/2025] Meta AI: I don’t understand Azerbaijani yet, but I’m working on it. I will send you a message when we can talk in Azerbaijani.
[4:33 pm, 22/10/2025] PPM 3: DeepSeek
[4:36 pm, 22/10/2025] PPM 1: Which LLM's in our regular usage have computer vision? Can we share it with those too?
[5:02 pm, 22/10/2025] PPM 3: Copilot
[5:04 pm, 22/10/2025] PPM 3: Differential diagnosis prioritized by likelihood and clinical relevance
- Bullosis diabeticorum — spontaneous, tense blisters occurring in patients with diabetes; can precede metabolic decompensation through stress or unrecognized infection.
- Bullous impetigo / staphylococcal infection — flaccid bullae with crusting that can seed bacteremia and trigger DKA as a stressor.
- Bullous drug reaction (including fixed drug eruption) — acute onset after new medication; can be widespread and precipitate systemic illness.
- Autoimmune bullous disease (bullous pemphigoid, pemphigus vulgaris) — clusters of tense or flaccid blisters; inflammatory burden can precipitate metabolic instability.
- Stevens-Johnson syndrome / toxic epidermal necrolysis spectrum — mucocutaneous erosions and widespread epidermal detachment that commonly cause severe systemic illness and metabolic derangement.
- Herpetic or varicella-zoster bullous infection — grouped vesiculobullous lesions that may cause systemic symptoms and secondary bacterial infection.
- Necrotizing soft-tissue infection with bullae (e.g., clostridial or streptococcal) or ecthyma gangrenosum — rapidly progressive, painful bullae with systemic toxicity and high risk of sepsis precipitating DKA.
- Traumatic or friction blisters with secondary infection — localized but can become systemic if infected.
---
Key clues from the images that support or argue against diagnoses
- Crusted scabs and mixed tense/flaccid-appearing lesions favor bacterial impetigo or secondary infection over classic bullosis diabeticorum.
- Localized forearm distribution without obvious mucosal lesions lowers immediate likelihood of SJS/TEN but does not exclude drug reactions or autoimmune disease.
- Evidence of inflammation and crusting increases concern for bacterial colonization that could trigger systemic inflammation and DKA.
---
Immediate diagnostic actions to prioritize now
1. Blood tests: CBC, CRP, blood cultures, blood glucose, electrolytes, renal function, venous blood gas.
2. Local sampling: Bacterial swab and culture with sensitivities from erosions or purulent areas; if vesicular, viral PCR for HSV/VZV.
3. Skin biopsy: Punch biopsy including perilesional skin for routine histology and direct immunofluorescence to evaluate autoimmune bullous disease.
4. Empiric sepsis evaluation: Assess for source control and early broad-spectrum antibiotics when systemic infection is suspected.
5. Medication review: Rapidly review recent drugs and exposures that could cause bullous drug reactions.
---
Immediate management priorities that affect both skin and DKA
- Treat DKA per protocol while simultaneously evaluating for sepsis because infection is a common precipitant.
- If signs of systemic infection or sepsis exist, start empiric IV antibiotics after obtaining cultures.
- Avoid empiric systemic steroids until infection is reasonably excluded if autoimmune bullous disease is suspected because steroids worsen uncontrolled infection and hyperglycaemia.
- Local wound care: gentle cleansing, sterile non-adherent dressings, and avoid unroofing intact tense blisters unless necessary for symptomatic reasons.
---
Red flags requiring urgent escalation
- Rapid extension of lesions, high fever, hemodynamic instability, severe pain disproportionate to exam, mucosal involvement, purulent drainage, crepitus, or signs of necrosis.
- Any red flag mandates immediate surgical and infectious disease input and consideration of ICU-level care.
---
Suggested next step I will assume you want and will provide now
I will prepare a concise one-page clinician checklist you can paste into the chart covering focused history questions, targeted exam points, orders (labs, cultures, biopsy), empiric medication options, and escalation triggers.[copilot]
[5:05 pm, 22/10/2025] PPM 3: Image overview
You uploaded two clinical photographs of a forearm showing multiple skin lesions including tense and flaccid blisters, crusted scabs, erythematous patches, and areas of post-inflammatory discoloration. The setting appears clinical and the arm is partially clothed by a blue checkered shirt.
Most likely causes to consider
- Bullous autoimmune blistering disease such as bullous pemphigoid or pemphigus vulgaris.
- Infectious blistering disorders including herpes simplex or varicella-zoster in atypical distribution.
- Contact or irritant dermatitis with superimposed secondary infection.
- Bullous drug reaction or fixed drug eruption.
- Trauma with secondary impetiginization.
Important red flags that need urgent attention
- Rapid expansion of blisters or involvement of large body surface area.
- Systemic signs: fever, malaise, hypotension, confusion, or tachycardia.
- Perioral, ocular, oral, or mucosal involvement.
- Signs of systemic infection at lesion sites: spreading cellulitis, increasing pain, purulent drainage, rapidly spreading erythema.
- Widespread epidermal detachment or suspected toxic epidermal necrolysis.
Immediate practical steps for safe care
- Keep the area clean and dry; avoid unroofing intact blisters.
- If blisters rupture, gently cleanse with saline and apply a non-adherent sterile dressing.
- Start topical antisepsis for open lesions and consider tetanus status review if traumatic.
- Avoid topical steroids or antibiotics unless prescribed by the treating clinician.
- If any red flags are present, arrange urgent in-person assessment or emergency care.
Recommended investigations to clarify diagnosis
- Full clinical skin examination including mucosal surfaces.
- Bacterial swab and culture from any purulent lesion for targeted antibiotics.
- Viral PCR from blister fluid if herpes or varicella is suspected.
- Skin biopsy with both routine histology and direct immunofluorescence for autoimmune blistering diseases.
- Basic labs: complete blood count, CRP or ESR, and metabolic panel if systemic illness suspected.
- Review recent medications and exposures for possible drug reaction.
What to tell the clinician or include in documentation
- Onset, progression timeline, and any preceding symptoms such as itch, pain, or fever.
- Recent new medications, vaccinations, or topical exposures.
- Any prior similar episodes, autoimmune disease history, or immunosuppression.
- Presence or absence of mucosal lesions and systemic symptoms.
- Photos with date and time and description of treatments already applied.
Short actionable plan
1. If any red flag present, seek urgent in-person care.
2. If stable, arrange dermatology review and same-day workup: wound culture, viral PCR if appropriate, and skin biopsy with immunofluorescence.
3. Document and photograph lesions serially for progression and treatment response.
If you want, I will convert the above into a one-page note for the chart, a patient-facing instruction sheet, or a checklist for the clinician to use during assessment.
[12:37 pm, 23/10/2025] PPM 2: What is his type of diabetes you think sir? @PPM1Sir
[12:59 pm, 23/10/2025] PPM 1: Good question. Hoping to review him in the afternoon closely again
[12.47 pm, 29/10/2025] PPM 1: EMR summary:As per HIPAA deidentification we need to think of a way to modify the time stamps by removing exact dates and replacing them with seasons, keeping just the year date intact. Instead of putting exact dates we can use day 1, to day n to indicate the patient timeline sequence. Also age in broad terms instead of exact age.
Age/Gender: Middle aged /Male
Address:
Discharge Type: Relieved
Admission Date: 17/10/2025 09:11 AM
Diagnosis
SEVERE ACUTE PANCREATITIS WITH MODS (ARDS, AKI, ALI)-RESOLVING
DIBETIC KETOACIDOSIS(RESOLVED)
DELIRIUM SECONDARY TO ALCOHOL WITHDRAWAL
DIABETICORUM BULLOSA
HEMEF WITH GRADE II DIASTOLIC DYSFUNCTION
DENOVO HTN
Case History and Clinical Findings
C/O PAIN ABDOMEN SINCE 4 DAYS
C/O SHORTNESS OF BREATHBSINCE 3 DAYS
C/O ALTERED SENSORIUM SINCE YESTERDAY NIGHT
HOPI; PATIENT WAS APPARENTLY ASYMPTOMATIC 4 DAYS AGO THEN HE DEVELOPED PAIN ABDOMEN AT RIGHT LOWER ABDOMEN (RIGHT ILIAC REGION), NON RADIATING, NO AGGREVATING FACTORS, RELIEVED ON MEDICATION. H/O SOB, INITIALLY GRADE II
MMRC, THEN PROGRESSED TO GRADE III, H/O 2-3 EPISODES OF VOMITINGS 4DAYS AGO
RESLOVED ON MEDICATION, NON BILIOUS, NON BLOODED TINGED, CONTAINING FOOD PARTICLES. H/O DECEASED URINE OUTPUT 4DAYS AGO RESOLVED AFTER TREATMENT. PATIENT WAS INITIALLY TAKEN TO A LOCAL PRIVATE HOSPITAL, WHERE HE WAS
ADMITTED MANAGED CONSERVATIVELY. H/OM 3-4 EPISODES OF LOOSE STOOLS 2DAYS
AGO, NOW RESOLVED. NO H/O CHEST PAIN, PALPITATION, BURNING MICTURITION,
SEIZURES, LOC, FEVER, COUGH.
Page-2
KIMS HOSPITALS
2
PAST HISTORY; K/C/O T2DM FOR 3DAYS ON INJ. MIXTARD 0-0-1., K/C/O CLD SINCE 2010
TREATED CONSERVATIVELY. H/O LEFT PLURAL EFFUSION S/P PLURAL TAPPING DONE IN
2014 H/O 1 O SDP TRANSFUSION ON 16/10/25, 4 O FFPS TRANSFUSION ON 15/10/25. H/O
INJ.MEROPENAM 1GM IV/BD GIVEN OUTSIDE AT 9.30PM. N/K/C/O HTN, TB. ASTHMA, CAD. EPILEPSY
PERSONAL HISTORY: MARRIED, LOST APPETITE, MIXED DIET, IRREGULAR BOWEL SINCE 3-
4 DAYS AND REGULAR BLADDER MOVEMENTS , NO KNOWN ALLERGIES , ALCOHOL -
CHRONIC ALCOHOLIC
GENERAL EXAMINATION: NO PALLOR , NO ICTERUS, NO CYANOSIS,NO CLUBBING,NO
LYMPHADENOPATHY, NO PEDAL EDEMA ,NO MALNUTRITION
VITALS:- TEMP: AFEBRILE, BP: 170/100MMHG, RR: 16CPM, PR:92 BPM, SPO2: 94% AT RA
SYSTEMIC EXAMINATION-CVS - S1 S2 +, NO MURMURS; RS - BAE +, NVBS, CREPTS IN LEFT MA, IAA; PER ABDOMEN -SOFT TENDER; CNS- NFND
SURGERY REFFERAL WAS DONE I/V/O BED SORE- DOCUMENTED AS NO BED SORE
PSYCHIATRY REFFERAL WAS DONE I/V/O DELIRIUM SECONDARY TO ALCOHOL WITHDRAL
AND ADVICED INL LORAZEPAM 1/2 AMPULE SOS
DERMATOLOGY REFFERAL WAS DONE I/V/O LEFT UPPER LIMB SWELLING ALONG WITH
FLUID FILLED BULLAE ASSOCIATED WITH PEELING OF SKIN AND ADVICED FUDIC CREAM FOR L/A
Investigation
17/10/25 HEMOGRAM HB-8.2, PCV 25.6, TLC 14600, RBC 3.2, PLC 33000.18/10/25 HEMOGRAM
HB 8.6, PCV 25.8, TLC 6920, RBC3.4 PLC 48000
19/10/25 HEMOGRAM HB 9.8, PCV 30.2, TLC 5750, RBC 3.89, PLC 70000 .20/10/25 HEMOGRAM
HB 8.7, PCV 26.5, TLC 8060, RBC 3.4 PLC 62000.
21/10/25 HB 8.7, PCV 26.5, TLC 8060, RBC 3.4 PLC 70000 .22/10/25 HB 8.2, PCV 24.4, TLC 9200
RBC 3.19 PLC 90000
23/10/25 HB 8.4, PCV 25.8, TLC 9570, RBC 3.3 PLC 72000
17/10/25 HBA1C- 8.2
17/10/25 PT-17, INR-1.2, APTT-35. BT-2.30SEC, CT-5 MIN (19/10/25) PT -18, INR-1.33, APTT-34
(22/10/25) PT-18, INR-1.33, APTT-35.
17/10/25CUE EPITHELIAL CELLS 2-3, PUS CELLS 2-4, RBS NIL, SUGARS-TRACE, ALB
TRACE<30MGMG/DL
Page-3
KIMS HOSPITALS
3
17/10/25 RFT UREA 116, CR 408, NA+ 145, K+4.7, CL- 105. (18/10/25) UREA 146, CR 4.3, NA+
145, K+ 4.1, CL- 109 (19/10/25) UREA 149, CR 3.8, NA+ 145, K+ 3.7, CL- 109 (20/10/25) UREA 145
CR 3.2, NA+ 146, K+ 3.5, CL- 104 (21/10/25) UREA 122, CR 1, NA+ 143, K+ 3.2, CL- 110 22/10/25
RFT UREA 77, CR 1.50, NA+ 143, K+ 3.4, CL- 106(23/10/25) UREA 49, CR 1.30, NA+ 141, K+ 3.3
, CL- 103(24/10/25) UREA 27, CR 1.6, NA+ 141, K+ 3.6, CL- 103
17/10/25 LFT TB 3.14, DB 1.38, SGPT 371, SGOT 202, ALP 184, TP 6.0, ALB 3.5, A/G
1.4;(18/10/25) TB 3.09, DB 1.45, SGPT 443, SGOT 398, TP 5.2, ALB 3.1, A/G 1.48 (19/10/25) TB
3.27, DB 1.87, SGPT 445, SGOT 395, ALP 198, TP 5.5, ALB 2.8, A/G1.04 (20/10/25) TB 3.77, DB
1.43, SGPT 321, SGOT 786, ALP 214, TP 4.7, ALB 2.67, A/G 1.32 (21/10/25) TB 3.27, DB 1.27
SGPT 346, SGOT 756, ALP 246, TP 4.7, ALB 2.66, A/G 1.3 22/10/25 LFT TB 3.68, DB 1.15, SGPT
271, SGOT 517, ALP 261, TP 4.7, ALB 2.7, A/G 1.35; (23/10/25) TB 3.07, DB 1.01, SGPT 206, SGOT
247, ALP 250, TP 5.1, ALB 2.7, A/G 1.13(24/10/25) TB 3.23, DB 1.17, SGPT 138, SGOT 102, ALP
223, TP 5.7, ALB 2.8, A/G 0.97
17/10/25 S. LIPASE 142. S. AMYLASE 216, S.LDH 2650
P. SMEAR -MICROCYTIC HYPOCHROMIC ANEMIA, THROMBOCYTOPENIA
ABG PROFILE; -
17/10/25 9:30AM PH-7.252, PCO2 12.6, PO2 84.7, HCO3- 5.4, SO2 96.6
4:00PM PH 7.193, PCO2 19, PO2 90, HCO3- 7.2, SO2 95.5
8:00PM PH 7.33, PCO2 18.3, PO2 93.3, HCO3 9.4, SO2 97.9
11:00PM PH 7.397, PCO2 22.2, PO2 103, HCO3 10.4, SO2 98.9
18/10/25 5:30AM PH 7.342, PCO2 27, PO2 40.4, HCO3- 14.2, SO2 74.2
19/10/25 5;30AM PH7.327, PCO2 33.2, PO2 36.3, HCO3 16.9, SO2 62.3
20/10/25 PH-7.305, PCO2-32, PO2-66.6, HCO3-15.5, SO2 89.8
21/10/25 PH-7.341, PCO2-30.8, PO2-66.1, HCO3-16.2, SO2-90.1
22 /10/25 PH-7.40, PCO2-27.6, PO2-125.1, HCO3-17, SO2-99
23 /10/25 PH-7.395, PCO2-29.4, PO2-47.3.1, HCO3-19, SO2-75.6
USG ABDOMEN - IMPRESSION -CHOLELITHIASIS, RIGHT MILD PLURAL EFFUSION WITH
COLLAPSE OF UNDERLYING LUNG FIELD
2D ECHO DONE ON 17/10/25
IMPRESSION ---'TACHY CARDIA'
-RWMA+ LAD HYPOKINETIC
-SEVERE TR + WITH MILD PAH ( RVSP 48+10258MMHG)
-MILD AR+ (AR-PHT 518M/SEC)
-MILD MR+ (ECCENTRIC TET MR); TRIVIAL PR+
-SCLEROTIC AV; NO AS/MS; IAS-INTACT
Page-4
KIMS HOSPITALS
-EF=45% MILD LV DYSFUNCTION +
-GRADE II DIASTOLIC DYSFUNCTION +
-MINIMAL PE+; NO LV CLOT
-IVC SIZE (1.78(MS)) DILATED NON COLLAPSING
-DILATED RA/RV
-RV DYSFUNCTION ; TAPSCE (1.85CM)
-NO LV CLOT ;NO VEGITATIONS
-IVS- JERKY MOVEMENTS
2D ECHO DONE ON 24/10/25
IMPRESSION - NO RWMA
-MILD TR ; NO PAH( RVSP 38+05243MMHG)
-TRIVIAL AR+ / MR + ; NO PR
-SCLEROTIC AV;NO AS/MS ; IAS-INTACT
-EF=61% GOOD LV SYSTOLIC FUNCTION
-GRADE I DIASTOLIC DYSFUNCTION +
-NO PE+ ; NO LV CLOT
-IVC SIZE (0.7 CMS ) COLLAPSING
- NORMAL SIZE ALL CHAMBERS
- NO RV DYSFUNCTION
Treatment Given (Enter only Generic Name)
IVF NS/RL AT 100ML/HR
INJ.MEROPENEM 5OOMG IN/BD
INJ.DOXYCYCLINE 100MG IV/BD
INJ.PAN 40MG IV/OD
INJ.VIT-K 1 AMP IV IN 100ML NS OVER 15 MINUTES
INJ.TRAMADOL 1 AMP IN 100ML NS IV/OD
INJ.HAI S/C TID ACC TO GRBS
INJ.THIAMINE 500MG IN/TID
SYP.LACTULOSE 20ML PO/HS
FUDIC CREAM L/A BD
NEOSPORIN POWER L/A
Advice at Discharge
TAB. PANTOP 40MG PO/OD 1-0-0 FOR 5 DAYS
TAB. THIAMINE 100MG PO/TID 1-1-1 FOR 5 DAYS
Page-5
KIMS HOSPITALS
5
TAB. DYTOR PLUS LS 10/25 PO/OD (8AM) 1-0-0 TO CONTINUE
TAB.METXL 25MG PO/OD (9AM) 1-0-0 TO CONTINUE
TAB. ECOSPIRIN AV 75/20MG PO/HS 0-0-1 TO CONTINUE
INJ. MIXTARD S/C BD 20U -X-15U TO CONTINUE
TAB . OLANZAPINE 2.5 MG PO/OD 0 - 0 - 1 FOR 5 DAYS
SYP. LACTULOSE 20ML PO/HS 0-0-20ML FOR 5 DAYS
FUDIC CREAM L/A BD
Follow Up
REVIEW TO GM AND PSYCHIATRY OP AFTER 5 DAYS OR SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
For Treatment Enquiries Patient/Attendant Declaration: - The medicines prescribed
and the advice regarding preventive aspects of care, when and how to obtain urgent care have been
explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER SIGNATURE OF PG/INTERNEE SIGNATURE OF
ADMINISTRATOR SIGNATURE OF FACULTY
Discharge Date
Date:24/10/25 Ward: MMW Unit: V
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