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I have been given this case to solve in an attempt to understand the topic of " Patient clinical data analysis" to develop my competancy in reading and comprehending clinical data including history, clinical finding, investigations and come up with a diagnosis and treatment plan.
Patient came to OPD with chief complaints of
* Abdominal distension since 10 days
*Bilateral pedal edema since 10 days,
* Decreased appetite since 4 days
* Decreased urine output since yesterday evening
Hopi:
Patient was apparently asymptomatic 6 months back then he had altered sensorium and decreased urine output and pedal edema for which he was admitted in a private hospital and got treated and his condition improved and was discharged.
2 months back he had trauma to the right leg ( fall due to giddiness while doing work)
The wound was non healing for which he went to local hospital and diagnosed with PAH
C/0 Abdominal distension which was diffuse not associated with abdominal pain ,local rise of temperature present,no tenderness, no vomitings
Bilateral Pedal edema which was gradually progressive pitting type extending upto knees.
since 4 days patient had decreased, appetite,
decreased urine output since yesterday evening (7.1.23)
h/o Malena present.
No history of fever, burning micturition,
Past history:
N/k/c/o DM, HTN,ASTHMA,TB, EPILEPSY.
Similar episodes 6 months ago
K/c/o PAH
GENERAL PHYSICAL EXAMINATION:
Patient was conscious,coherent
non cooperative,well oriented to time place and person
Vitals :
Temp: Afebrile
BP:110/70MMHG
PR: 105BPM
Spo2: 95%@RA
RR:20CPM
Pallor +
Icterus, cyanosis, clubbing, lymphadenopathy absent
Pedal edema +
Systemic examination:
CVS: S1;S2+,no murmurs
RS: BAE +
PER ABDOMEN:
INSPECTION:
Abdomen was distended with flanks full.
Umbilicus central and everted and slit like.
visible abdominal veins.
All quadrants of abdomen moving equally with respiration.
No scars, sinuses and peristalsis.
PALPATION:
Soft and Non tender.
No local rise in temperature.
Liver and spleen could not be palpable.
Hernial orifices are normal on both sides.
Measurements:
Abdominal girth: 84 cms.
Xiphisternum to umbilical length: 24 cms.
Umbilicus to public symphysis length: 18 cms.
PERCUSSION:
Liver dullness: upper border at 5 th right intercostal space in mid clavicular line. Lower border could not be assessed.
Spleen dullness: dullness noted in 8th intercostal space at mid axillary line.
Fluid thrill present.
AUSCULTATION :
Normal bowel sounds were heard.
Diagnosis:
HEPATIC ENCEPHALOPATHY SECONDARY TO ? ACUTE DECOMPENSATED LIVER DISEASE . GROSS ASCITIS WITH THROMBOCYTOPENIA,ACUTE KIDNEY INJURY
Investigations:
On 8/1/23
9/1/23
10/1/23
Chest x ray :
TREATMENT Salt restriction <2gms/day
Fluid restriction <1 liter /day
Syp.lactulose 15ml/day
Tab.Aldactone 50 mg/day
Tab.lasix 40 mg/day If SBP >100 mmhg
Inj.KCL 2 amp in 500 ml Ns over 5 hrs iv stat
2-3 egg whites/day
Tab.Thiamine 100mg/day
Abdominal girth measurement daily at 8:00am
Monitor vitals 4 th hourly
A 60-year male, brought to casualty with complaints of abdominal distension, bilateral pedal edema of grade II and decreased urine output since yesterday (07/01/2023) evening. Vitals at presentation were PR 105 bpm, RR 19 cpm, BP 110/70 mmHg, Spo2 94% @room air, GRBS 54 mg/dl; Upon arrival to casualty 1 unit of 25% dextrose was given following which his GRBS was 124 mg/dl. All necessary investigations were done and patient was shifted to ICU. The patient has become irritable and confused. Intravenous Thiamine was started. Diagnostic and therapeutic Ascitic tap was done under strict asceptic condition and samples were sent for analysis; 1 liter of ascitic fluid was removed and procedure was uneventful. Meanwhile his investigations showed serum pottasium of 2.4 mEq/L for which 20 mEq of pottasium correction was given. On 09/01/2023 the patient was Non coherent and Non cooperative, confused and irritable. His serum pottasium levels were 2 mEq/L for which pottasium correction was done. Therapeutic ascitic tap was done and around 1.5 liters of fluid was removed and the procedure was uneventful. His serum pottasium levels after correction was 2.1 mEq/L and started on 40 mEq/L pottasium correction. On 10/01/2023 around at 5:30 AM, patient BP and PR are not recordable with absent central and peripheral pulses and ECG showing pulseless electrical activity, CPR was started immediately according to ACLS guidelines, meanwhile patient was intubated. After few minutes of CPR, ECG monitor showed Polymorphic ventricular tachycardia and DC Shock of 200J was given, as Ventricular tachycardia was not reverted CPR was continued and 360J DC Shock was given, Intravenous Xylocaine 5ml and Magnesium sulphate of 2gram was given; CPR was continued and ventricular tachycardia not reverted another DC Shock of 360J was given, even after 40 minutes of CPR, ROSC was not attained. Inspite of all resuscitatory efforts he was not be revived and declared dead at 6:13 AM on 10/01/2023 as ECG showed flat line with no electrical activity.
IMMEDIATE CAUSE OF DEATH:
VENTRICULAR TACHYCARDIA SECONDARY TO REFRACTORY HYPOKALEMIA.
ANTECEDENT CAUSE OF DEATH:
1. DECOMPENSATED CHRONIC LIVER DISEASE .
2. ANEMIA WITH THROMBOCYTOPENIA.
3. HYPOKALEMIA.
4. ACUTE KIDNEY INJURY.
