Bed 6A — Naikashi, 52F

?SAIO + HCV Reactive

Clinical Interpretation

GCS E1V1M1 = GCS 3 — Deeply Unresponsive

• Bacterial overgrowth → increased gut ammonia production
• Constipation → delayed ammonia clearance
• Possible electrolyte disturbance

• Hepatic encephalopathy (most likely given HCV reactive)
• Hypertensive encephalopathy (SBP was 180/100 — now treated)
• Metabolic encephalopathy (electrolyte, glucose, uremia)
• Septic encephalopathy (source could be gut)
• Intracranial bleed/event (must rule out with CT brain)

Current Vitals Assessment

Note: Post-labetalol BP is now 130/90. Labetalol is appropriate for hypertensive emergency — watch for bradycardia and do NOT give if bronchospasm/heart block. Continue BP monitoring every 15–30 min. Target SBP 160 initially (avoid rapid overcorrection in suspected hypertensive encephalopathy).

Immediate Priorities

1. Airway / Neuroprotection

• GCS 3 → High aspiration risk
• Keep NPO, head end elevated 30°
• Consider elective intubation/ICU referral if GCS does not improve rapidly
• Call anesthesia/intensivist early

2. Rule Out Structural Cause

• Urgent CT Brain (non-contrast) — to exclude hemorrhagic stroke, bleed, herniation
• If CT clear → proceed with metabolic workup

3. Investigations

4. SAIO Management

• NGT insertion + free drainage — decompress the gut
• Strict NPO
• IV fluids (NS or RL) — correction of dehydration/electrolytes
• Monitor urine output (target >0.5 mL/kg/hr) → consider Foley catheter
• Serial abdominal exams — watch for peritonitis, perforation
• Surgical consult — for definitive SAIO management if conservative fails
• Avoid opioids if hepatic encephalopathy suspected (↑ sedation, ↑ ammonia indirectly)

5. Hepatic Encephalopathy Management (if ammonia elevated / CT brain normal)

• Lactulose 30–45 mL every 2 hours via NGT until loose stools (target 2–4 stools/day), then TDS
• Consider Rifaximin 550 mg BD (reduces gut ammonia-producing bacteria)
• Correct precipitants: electrolytes (K⁺, Na⁺), infection, GI bleed screen
• Avoid hepatotoxic drugs, benzodiazepines, opioids
• Protein restriction is no longer recommended routinely — maintain nutrition via NGT

6. Hypertension Management (ongoing)

• Post-labetalol: continue monitoring BP Q15–30 min
• If BP rises again: can repeat Inj Labetalol 10–20 mg IV (max 300 mg/day), or switch to Inj Nitroglycerin/Nicardipine IV infusion if persistent emergency
• Target: gradual reduction, not aggressive — SBP 150–160 in first hour

Summary — Working Diagnosis

Hepatic Encephalopathy Grade IV (GCS 3) likely secondary to decompensated HCV-related chronic liver disease, precipitated by Subacute Intestinal Obstruction + possible hypertensive encephalopathy component (SBP 180).

IMMEDIATE ACTIONS — Do RIGHT NOW

🔴 Step 1 — Airway (Most urgent)

• Call for help / activate emergency response NOW
• GCS 3 = no airway protection — high aspiration risk
• Position: left lateral decubitus or 30° head-up
• Have suction ready at bedside
• Call anesthesia for emergency intubation — don't wait

🔴 Step 2 — Check reversible causes immediately (at bedside)

Why GCS is Falling — Think in Order

1. Hypoglycemia — check glucose NOW, easiest fix
2. Worsening hepatic encephalopathy — ammonia accumulation (SAIO worsening gut stasis)
3. Hypertensive encephalopathy / Cerebral bleed — SBP was 180, labetalol given
4. Post-labetalol hypotension — overcorrection can drop cerebral perfusion
5. Sepsis — gut source from obstruction
6. CO2 narcosis — if underlying respiratory compromise

Escalation — Do Simultaneously

• Inform senior/attending IMMEDIATELY — this patient may need ICU transfer
• CT Brain STAT — once airway is secured/stable
• Insert Foley catheter — monitor UO
• NGT — decompress, but only after airway is confirmed safe
• Draw bloods: ABG, glucose, ammonia, LFT, electrolytes, CBC, INR, lactate

Bottom line: Falling GCS = presumed airway compromise until proven otherwise. Secure the airway first, find the cause second. Do not leave this patient alone. Call your senior now.