4.3 Renal and Hepatic Emergencies in Transport

4.3 Renal and Hepatic Emergencies in Transport

Acute Kidney Injury (AKI) Etiologies & Staging

Acute Kidney Injury (AKI) is characterized by a rapid decline in glomerular filtration rate (GFR), resulting in the accumulation of nitrogenous waste products (blood urea nitrogen [BUN] and serum creatinine) and dysregulation of fluid, electrolyte, and acid-base homeostasis.

Etiological Categories

1. Prerenal Azotemia: Caused by renal hypoperfusion without cellular parenchymal damage (e.g., severe hypovolemia, septic shock, heart failure, renal artery stenosis). Fractional excretion of sodium ($\text{FENa}$) is typically $< 1%$, and $\text{BUN}:\text{Creatinine}$ ratio is $> 20:1$.
2. Intrinsic / Intrarenal AKI: Caused by direct structural injury to the glomeruli, tubules, or interstitium. Acute Tubular Necrosis (ATN) from prolonged ischemia or nephrotoxins (aminoglycosides, iodinated contrast, rhabdomyolysis myoglobin) is the most common cause. $\text{FENa} > 2%$, $\text{BUN}:\text{Creatinine} < 15:1$, with muddy brown granular casts in urine sediment.
3. Postrenal AKI: Caused by urinary tract obstruction downstream of the kidneys (e.g., bilateral ureteral obstruction, prostatic hypertrophy, neurogenic bladder, obstructed Foley catheter).

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AKI Staging Criteria: RIFLE vs. KDIGO

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Emergency Hyperkalemia Management Protocol

Hyperkalemia ($[\text{K}^+] > 5.0\text{ mEq/L}$) is a life-threatening complication of renal failure. Severe hyperkalemia ($[\text{K}^+] > 6.5\text{ mEq/L}$) alters resting membrane potentials, risking lethal arrhythmias.

ECG Evolution in Hyperkalemia

1. $5.5 - 6.0\text{ mEq/L}$: Narrow, tall, peaked T waves.
2. $6.0 - 7.0\text{ mEq/L}$: PR interval prolongation, flattening of P waves, ST-segment depression.
3. $7.0 - 8.0\text{ mEq/L}$: QRS complex widening, loss of P waves.
4. $> 8.0\text{ mEq/L}$: QRS merges with T wave creating a classic sine-wave pattern, culminating in ventricular fibrillation or asystole.

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Multi-Tiered Hyperkalemia Interventions

Transport Pearl: Calcium stabilizes the myocardium but does NOT reduce total serum potassium. Always follow calcium administration immediately with intracellular shifting agents (Insulin + Dextrose, Albuterol).

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End-Stage Renal Disease (ESRD) & Vascular Access Precautions

Patients with ESRD rely on permanent vascular access for hemodialysis:

• Arteriovenous (AV) Fistula: Surgical anastomosis connecting a native artery directly to a vein (e.g., radiocephalic). Preferred due to lower infection and thrombosis rates.
• Arteriovenous (AV) Graft: Synthetic polytetrafluoroethylene (PTFE) conduit bridging an artery and vein.

Transport Management Precautions

1. Strict Arm Restrictions: NEVER obtain non-invasive blood pressure, perform venipuncture, or establish IV access in the extremity containing an AV fistula or graft. Pressure occlusion causes graft thrombosis or fistula rupture.
2. Vascular Access Assessment: Palpate for a continuous thrill (vibratory sensation) and auscultate for a continuous bruit (machinery murmur) every shift and post-transfer. Absence of thrill/bruit indicates access thrombosis.
3. Hemostasis Control: If an AV fistula ruptures or bleeds during transport, apply direct digital pressure immediately just proximal and distal to the bleeding site. Avoid circumferential tourniquets if possible, as they destroy the shunt.
4. Dialysis Disequilibrium Syndrome (DDS): Occurs during or shortly after hemodialysis due to rapid removal of urea from the intravascular space, creating a concentration gradient that shifts water into brain tissue. Manifests as headache, nausea, muscle cramps, confusion, seizures, and increased ICP. Treat with hypertonic saline or mannitol.

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Continuous Renal Replacement Therapy (CRRT) Considerations

Transporting critically ill patients maintained on Continuous Renal Replacement Therapy (CRRT) requires specialized vigilance:

• Modalities: Continuous Venovenous Hemofiltration (CVVH - convection), Continuous Venovenous Hemodialysis (CVVHD - diffusion), and Continuous Venovenous Hemodiafiltration (CVVHDF - combined).
• Circuit Pressure Monitoring: Monitor Filter Pressure, Access (Arterial) Pressure, Return (Venous) Pressure, and Transmembrane Pressure (TMP). A rising TMP indicates impending filter clotting.
• Dual-Lumen Catheter Maintenance: Large-bore hemodialysis catheters (VasCath/PermCath) placed in the internal jugular or femoral vein must NEVER be accessed for routine IV fluid or medication administration unless during cardiac arrest or explicit protocol clearance.

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Hepatic Encephalopathy, Hyperammonemia & Hepatorenal Syndrome

Hepatic encephalopathy is a reversible neuropsychiatric syndrome complicating acute liver failure or advanced cirrhosis. It results from the liver's inability to metabolize nitrogenous toxins absorbed from the gut—principally ammonia ($NH_3$).

Clinical Staging (West Haven Criteria)

• Grade 1: Euphoria or anxiety, mild confusion, impaired attention, slurred speech, subtle asterixis (flapping tremor).
• Grade 2: Lethargy, disorientation to time, inappropriate behavior, obvious asterixis.
• Grade 3: Somnolence to semi-stupor, responsive to verbal stimuli, profound confusion, gross disorientation.
• Grade 4: Coma (unresponsive to painful stimuli), decerebrate or decorticate posturing.

Pharmacological Management Protocol

1. Lactulose: Non-absorbable disaccharide administered $20 - 30\text{ g}$ PO/NG every 2-4 hours (or as a retention enema). Gut bacteria metabolize lactulose into lactic and acetic acids, acidifying the colonic lumen. Acidic pH converts gaseous ammonia ($NH_3$) into non-absorbable ammonium ($NH_4^+$), trapping it in the bowel. It also acts as an osmotic laxative to purge nitrogenous compounds. Target: 2-3 soft stools per day.
2. Rifaximin: Non-absorbable antibiotic ($550\text{ mg}$ PO BID) that eradicates ammonia-producing colonic bacteria (e.g., E. coli).
3. Cerebral Edema in Acute Liver Failure: Hyperammonemia causes astrocyte swelling and intracranial hypertension. Maintain head of bed at $30^\circ$, maintain $\text{PaCO}_2$ $35-40\text{ mmHg}$, and infuse hypertonic saline to maintain target serum sodium $145-150\text{ mEq/L}$.

Hepatorenal Syndrome (HRS)

Hepatorenal syndrome is functional renal failure occurring in severe liver disease caused by intense splanchnic arterial vasodilation, which leads to severe renal vasoconstriction and renal hypoperfusion.

• Type 1 HRS: Rapidly progressive renal failure (doubling of baseline serum creatinine to $> 2.5\text{ mg/dL}$ in $< 2\text{ weeks}$). High mortality.
• Management Strategy: Combine splanchnic vasoconstrictors (Terlipressin, Norepinephrine, or Octreotide + Midodrine) with continuous IV Albumin ($1\text{ g/kg}$ on day 1, followed by $20-40\text{ g/day}$) to expand intravascular volume, increase mean arterial pressure, and reverse renal vasoconstriction.