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SURGICAL CRITICAL CARE

SURGICAL CRITICAL CARE. Gastrointestinal System Acute Renal Failure Hepatic Dysfunction. Gastrointestinal System. Stress Gastritis Abdominal Compartment Syndrome Nutritional Support. Pathophysiology of Stress Gastritis. Hypovolemia Decreased Cardiac Output Splanchnic hypoperfusion

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SURGICAL CRITICAL CARE

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  1. SURGICAL CRITICAL CARE Gastrointestinal System Acute Renal Failure Hepatic Dysfunction

  2. Gastrointestinal System • Stress Gastritis • Abdominal Compartment Syndrome • Nutritional Support

  3. Pathophysiology of Stress Gastritis • Hypovolemia • Decreased Cardiac Output • Splanchnic hypoperfusion • Acid back-diffusion, bicarbonate hyposecretion, decreased mucosal blood flow and depressed gastric motility… Mucosal Erosion

  4. Stress Gastritis / Gastric Ulceration • Risk factors • Mechanical ventilation > 48hrs • Coagulopathy • Significant Burns • Head Injury / Brain Insult • Organ Transplantation / Immunosuppression • High dose steroids • Major Surgery, pancreatitis, renal failure, hepatic failure, multiple traumatic injuries.

  5. Prophylaxis • Enteral Feeding ( >50% of caloric intake goal) • Sucralfate (sucrose based polymer) • Histamine-2 receptor antagonists • Proton pump inhibitors Sucralfate (good protection-hinders absorbtion) H2 Blockers - 60% acid suppression PPI – 100% acid suppression Our preference is ________.

  6. Abdominal Compartment Syndrome ‘Increased intra-abdominal pressure’ • Massive abdominal or pelvic hemorrhage • Circumferential burn eschar • Reduction of large ventral hernia • Bowel distention secondary to obstruction • Prolonged evisceration • Gut ischemia Edema narrowing mesenteric veins and lymphatics

  7. Abdominal Compartment Syndrome • Cardiovascular – decrease Cardiac Index • Pulmonary – decrease pulmonary compliance due to high airway pressures • Renal – parenchymal compression & ↓ RBF Signs - Abdominal distention - Oliguria - Hypoxia with high airway pressures

  8. Abdominal Compartment Syndrome Bladder pressure accepted as subjective approximation to intra-abdominal pressure Grade Intra-abdominal pressure Treatment I 10-14 mmhg Resusc. II 15-24 mmhg Resusc. III 25-35 mmhg Decompression IV > 35 mmhg Emergent re-exploration

  9. Nutritional Support • Neuroendocrine response to critical illness: - Release of stress hormones(epinephrine, glucagon & cortisol) - These coupled with inflammatory mediators leave the patient in a hypercatabolic state – visceral protein erosion and depleting glucose and fat stores. • Nutritional Support required 1- Lack of nutrition > 5-7 days 2- Duration of illness expected to exceed 10 days 3- Malnourished patient (serum protein levels)

  10. Nutrition • Types 1. Enteral Nutrition ( Fine Bore NGT: Dubhoff ) 2. Total Parenteral Nutrition 3. Peripheral Parenteral Nutrition **Best place to place Dubhoff is the duodenum: Decreased aspiration risk (Keeps the stomach empty) Reach the TF goal sooner Small bowel function usually remains despite stomach and colonic hypomotility.

  11. Nutrition • How much to give? 2000-2500 kcal/day Basal energy expenditure (kcal/day) BEE=66+(13.7x weight) + (5 x height) – (6.8 x age) males BEE=65+(9.6x weight) + (1.8 x height) – (4.7 x age) females Multiply by ‘Stress factor’ approx. 1.5 • 2.5g protein/kg/day (1g normal) • Monitor using Pre-albumin levels (range 16-35 mg/dl) Prealbumin - monitor every 5 days - half life 1-2 days (albumin 20 days) - falsely elevated with steroids and renal failure

  12. Acute Renal Failure • High mortality >50% in the ICU setting • Classification • Prerenal • Renal • Post Renal First signs are oliguria (<400cc/24hrs) and rise in creatinine levels. ( 30-40% of ARF is non-oliguric)

  13. Acute Renal Failure Prerenal Hypotension: Hemorrhage, Sepsis, CP bypass ↓ RBF: Instrumental, trauma, inotropes, CHF Renal Acute Tubular Necrosis, pigment nephropathy (Contrast, NSAIDS, aminoglycosides, myoglobin, ampho. B) Post-Renal Single kidney obstruction / BPH / Bladder Stones / Urethral Tumour / Congenital

  14. Example • Post AAA repair ARF, causes may be: • Cross clamping • Sympathetic activation with manipulation • Emboli • Washout acidosis after lower extremity reperfusion • Hypovolemia • Post renal obstruction from hematoma Note: Autoregulation keeps adequate RBF to a systemic arterial pressure above 90mmhg. This is achieved by norepinephrine and angiotensin.

  15. Physiology / Pathophysiology • Normal physiology of nephron in mind • Pathophysiology of ARF - Initial injury is ischemia or toxin deposition: -Tubular injury (reversible) -Cortical injury (irreversible) Mechanism: Vasoconstriction and altered glomerular permeability ‘pigment deposition, retrograde pressure/tubular blockage, luminal edema’ • Alterations in ARF • Metabolic acidosis • Hyperkalemia • Hyperphophatemia • Hypocalcemia • Hyponatremia • Hypermagnesemia

  16. Acute Renal Failure • High mortality • Prolonged recovery course • Complication of renal replacement therapy PREVENTION

  17. Acute Renal Failure • Monitor Urine output (Foley catheter) • Blood pressure measurement (invasive monitoring) • Volume Status (sensible and insensible losses) • Monitor urea, creatinine and electrolytes • Urinalysis (casts, crystals, mucus, RBCs) • Urine Osmolality and Electrolytes

  18. ARF – measurements & calculations

  19. Fractional Excretion of Sodium FE Na = excreted Na / filtered Na FE Na = UNa/PNa x Pcreat / Ucreat

  20. ARF - Treatment • Fluid management • Correct electrolytes • Diuretics • Renal Replacement Therapy • Hemodialysis • Continuous Venovenous Hemodialysis • Continuous Arteriovenous Hemodialsys

  21. Prevention of ARF is much easier, more cost effective, and more successful than its treatment Fluid balance, proper medications, avoid nephrotoxic drugs. ‘Contrast material causes 10% of hospital acquired ARF’

  22. Hepatic Dysfunction • Primary • Secondary may be seen in ICU setting • Acute exacerbation of chronic liver disease Jaundice, impaired synthetic activity-coagulation disorder, electrolyte imbalance, altered mental status-cerebral edema, renal and pulmonary dysfunction, hepatorenal syndrome, ascites-spontaneous bacterial peritonitis, multi-organ failure.

  23. Hepatic Dysfunction - Management • Reversal of precipitating factors • Removal of offending drugs • Correcting fluid/electrolyte abnormalities • Treating infections • Ammonia elimination by administering lactulose and/or neomycin. • Adequate nutrition (sodium/protein restriction) • Address coagulopathy

  24. Hepatorenal Syndrome • Renal dysfunction seen in approx. 40% of patients in fulminant hepatic failure • Mechanisms seems to be related to renal vasoconstriction • Characterized by azotemia, oliguria, low urinary sodium (<10mEq/L) and high urine osmolality • Poor prognosis – improvements seen using terlipressin (vasopressin analogue) • Kidneys not permanently damaged.

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