SURGICAL SURGICAL CRITICAL CARECRITICAL CARE

Gastrointestinal SystemGastrointestinal System

Acute Renal FailureAcute Renal Failure

Hepatic DysfunctionHepatic Dysfunction

Gastrointestinal SystemGastrointestinal System

Stress GastritisStress Gastritis

Abdominal Compartment SyndromeAbdominal Compartment Syndrome

Nutritional SupportNutritional Support

Pathophysiology of Stress Pathophysiology of Stress GastritisGastritis

HypovolemiaHypovolemia Decreased Cardiac OutputDecreased Cardiac Output Splanchnic hypoperfusionSplanchnic hypoperfusion• Acid back-diffusion, bicarbonate Acid back-diffusion, bicarbonate

hyposecretion, decreased mucosal hyposecretion, decreased mucosal blood flow and depressed gastric blood flow and depressed gastric motility… motility…

Mucosal ErosionMucosal Erosion

Stress Gastritis / Gastric Stress Gastritis / Gastric UlcerationUlceration

Risk factorsRisk factors Mechanical ventilation > 48hrs Mechanical ventilation > 48hrs CoagulopathyCoagulopathy Significant BurnsSignificant Burns Head Injury / Brain Insult Head Injury / Brain Insult Organ Transplantation / Organ Transplantation /

ImmunosuppressionImmunosuppression High dose steroidsHigh dose steroids Major Surgery, pancreatitis, renal failure, hepatic failure, Major Surgery, pancreatitis, renal failure, hepatic failure,

multiple traumatic injuries.multiple traumatic injuries.

ProphylaxisProphylaxis Enteral Feeding ( >50% of caloric intake Enteral Feeding ( >50% of caloric intake

goal)goal) Sucralfate (sucrose based polymer)Sucralfate (sucrose based polymer) Histamine-2 receptor antagonistsHistamine-2 receptor antagonists Proton pump inhibitorsProton pump inhibitors

Sucralfate (good protection-hinders absorbtion)Sucralfate (good protection-hinders absorbtion)H2 Blockers - 60% acid suppressionH2 Blockers - 60% acid suppressionPPI – 100% acid suppressionPPI – 100% acid suppression

Our preference is ________.Our preference is ________.

Abdominal Compartment Abdominal Compartment SyndromeSyndrome

‘ ‘Increased intra-abdominal pressure’Increased intra-abdominal pressure’• Massive abdominal or pelvic hemorrhageMassive abdominal or pelvic hemorrhage• Circumferential burn escharCircumferential burn eschar• Reduction of large ventral herniaReduction of large ventral hernia• Bowel distention secondary to obstructionBowel distention secondary to obstruction• Prolonged eviscerationProlonged evisceration• Gut ischemia Gut ischemia

EdemaEdema narrowing mesenteric veins and narrowing mesenteric veins and

lymphaticslymphatics

Abdominal Compartment Abdominal Compartment SyndromeSyndrome

Cardiovascular – decrease Cardiac IndexCardiovascular – decrease Cardiac Index Pulmonary – decrease pulmonary compliance Pulmonary – decrease pulmonary compliance

due to high airway pressures due to high airway pressures Renal – parenchymal compression & ↓ RBFRenal – parenchymal compression & ↓ RBF

SignsSigns- Abdominal distention- Abdominal distention- Oliguria- Oliguria- Hypoxia with high airway pressures- Hypoxia with high airway pressures

Abdominal Compartment Abdominal Compartment SyndromeSyndrome

Bladder pressure accepted as subjective Bladder pressure accepted as subjective approximation to intra-abdominal pressureapproximation to intra-abdominal pressure

GradeGrade Intra-abdominal pressure Intra-abdominal pressure TreatmentTreatment

II 10-14 mmhg10-14 mmhg Resusc.Resusc.

IIII 15-24 mmhg15-24 mmhg Resusc.Resusc.

IIIIII 25-35 mmhg25-35 mmhg DecompressionDecompression

IVIV > 35 mmhg> 35 mmhg Emergent re-Emergent re-explorationexploration

Nutritional SupportNutritional Support• Neuroendocrine response to critical illness:Neuroendocrine response to critical illness:

- - Release of stress hormonesRelease of stress hormones (epinephrine, glucagon & (epinephrine, glucagon & cortisol)cortisol)

- These coupled with inflammatory mediators leave the - These coupled with inflammatory mediators leave the patient in a hypercatabolic state – visceral protein patient in a hypercatabolic state – visceral protein erosion and depleting erosion and depleting glucose glucose and fat stores.and fat stores.

• Nutritional Support Nutritional Support requiredrequired

1- Lack of nutrition > 5-7 days1- Lack of nutrition > 5-7 days

2- Duration of illness expected to exceed 10 2- Duration of illness expected to exceed 10 daysdays

3- Malnourished patient (serum protein 3- Malnourished patient (serum protein levels)levels)

NutritionNutrition

Types Types

1. Enteral Nutrition ( Fine Bore NGT: 1. Enteral Nutrition ( Fine Bore NGT: Dubhoff )Dubhoff )

2. Total Parenteral Nutrition 2. Total Parenteral Nutrition

3. Peripheral Parenteral Nutrition3. Peripheral Parenteral Nutrition

**Best place to place Dubhoff is the duodenum:**Best place to place Dubhoff is the duodenum:

Decreased aspiration risk (Keeps the stomach empty)Decreased aspiration risk (Keeps the stomach empty)

Reach the TF goal soonerReach the TF goal sooner

Small bowel function usually remains despite stomach and Small bowel function usually remains despite stomach and colonic hypomotility. colonic hypomotility.

NutritionNutrition How much to give? How much to give? 2000-2500 kcal/day2000-2500 kcal/day

Basal energy expenditure (kcal/day)Basal energy expenditure (kcal/day)BEE=66+(13.7x weight) + (5 x height) – (6.8 x age) BEE=66+(13.7x weight) + (5 x height) – (6.8 x age) malesmales

BEE=65+(9.6x weight) + (1.8 x height) – (4.7 x age) BEE=65+(9.6x weight) + (1.8 x height) – (4.7 x age) femalesfemales

Multiply by ‘Stress factor’ approx. 1.5Multiply by ‘Stress factor’ approx. 1.5• 2.5g protein/kg/day (1g normal)2.5g protein/kg/day (1g normal)• MonitorMonitor using Pre-albumin levels using Pre-albumin levels (range 16-35 (range 16-35

mg/dl)mg/dl)

PrealbuminPrealbumin - monitor every 5 days - monitor every 5 days

- half life 1-2 days - half life 1-2 days (albumin (albumin 20 days)20 days)

- falsely elevated with steroids and - falsely elevated with steroids and renal renal failure failure

Acute Renal FailureAcute Renal Failure

High mortality >50% in the ICU settingHigh mortality >50% in the ICU setting ClassificationClassification

PrerenalPrerenal RenalRenal Post RenalPost Renal

First signs are oliguria (<400cc/24hrs) and First signs are oliguria (<400cc/24hrs) and rise in creatinine levels. ( 30-40% of ARF is rise in creatinine levels. ( 30-40% of ARF is non-oliguric)non-oliguric)

Acute Renal FailureAcute Renal FailurePrerenalPrerenal

Hypotension: Hemorrhage, Sepsis, CP Hypotension: Hemorrhage, Sepsis, CP bypass ↓ RBF: Instrumental, trauma, bypass ↓ RBF: Instrumental, trauma, inotropes, CHFinotropes, CHF

Renal Renal

Acute Tubular Necrosis, pigment Acute Tubular Necrosis, pigment nephropathynephropathy

(Contrast, NSAIDS, aminoglycosides, myoglobin, ampho. (Contrast, NSAIDS, aminoglycosides, myoglobin, ampho. B)B)

Post-RenalPost-Renal

Single kidney obstruction / BPH / Bladder Single kidney obstruction / BPH / Bladder Stones / Urethral Tumour / CongenitalStones / Urethral Tumour / Congenital

ExampleExample Post AAA repair ARF, causes may be:Post AAA repair ARF, causes may be:

Cross clampingCross clamping Sympathetic activation with manipulationSympathetic activation with manipulation EmboliEmboli Washout acidosis after lower extremity reperfusionWashout acidosis after lower extremity reperfusion HypovolemiaHypovolemia Post renal obstruction from hematomaPost renal obstruction from hematoma

Note: Autoregulation keeps adequate RBF Note: Autoregulation keeps adequate RBF to a systemic arterial pressure above to a systemic arterial pressure above 90mmhg.90mmhg.

This is achieved by norepinephrine and This is achieved by norepinephrine and angiotensin.angiotensin.

Physiology / Physiology / PathophysiologyPathophysiology

Normal physiology of nephron in mindNormal physiology of nephron in mind Pathophysiology of ARFPathophysiology of ARF

- Initial injury is ischemia or toxin deposition:- Initial injury is ischemia or toxin deposition:-Tubular injury (reversible)-Tubular injury (reversible)-Cortical injury (irreversible)-Cortical injury (irreversible)

Mechanism: Vasoconstriction and altered glomerular Mechanism: Vasoconstriction and altered glomerular permeability permeability ‘pigment deposition, retrograde pressure/tubular ‘pigment deposition, retrograde pressure/tubular blockage, luminal edema’blockage, luminal edema’

Alterations in ARFAlterations in ARF Metabolic acidosisMetabolic acidosis HyperkalemiaHyperkalemia HyperphophatemiaHyperphophatemia HypocalcemiaHypocalcemia HyponatremiaHyponatremia HypermagnesemiaHypermagnesemia

Acute Renal FailureAcute Renal Failure

High mortalityHigh mortality Prolonged recovery courseProlonged recovery course Complication of renal replacement Complication of renal replacement

therapytherapy

PREVENTIONPREVENTION

Acute Renal FailureAcute Renal Failure Monitor Urine output (Foley catheter)Monitor Urine output (Foley catheter) Blood pressure measurement (invasive Blood pressure measurement (invasive

monitoring)monitoring) Volume Status (sensible and Volume Status (sensible and

insensible losses)insensible losses) Monitor urea, creatinine and Monitor urea, creatinine and

electrolyteselectrolytes Urinalysis (casts, crystals, mucus, Urinalysis (casts, crystals, mucus,

RBCs)RBCs) Urine Osmolality and ElectrolytesUrine Osmolality and Electrolytes

ARF – measurements & ARF – measurements & calculationscalculations

Prerenal Prerenal AzotemiaAzotemia

Tubular Tubular InjuryInjury

Urine Urine OsmolalityOsmolality

> 500> 500 < 350< 350

U/P U/P OsmolalityOsmolality

>1.25>1.25 <1.1<1.1

U/P U/P creatininecreatinine

> 40> 40 < 20< 20

U/P ureaU/P urea >8>8 < 3< 3

Urine sodiumUrine sodium <20<20 >40>40

FE NaFE Na <1<1 >3>3

Fractional Excretion of Fractional Excretion of SodiumSodium

FE Na = excreted Na / filtered NaFE Na = excreted Na / filtered Na

FE Na = UFE Na = UNaNa/P/PNaNa x P x Pcreatcreat / / UUcreatcreat

ARF - TreatmentARF - Treatment

Fluid managementFluid management Correct electrolytesCorrect electrolytes DiureticsDiuretics Renal Replacement TherapyRenal Replacement Therapy

HemodialysisHemodialysis Continuous Venovenous HemodialysisContinuous Venovenous Hemodialysis Continuous Arteriovenous Continuous Arteriovenous

HemodialsysHemodialsys

Prevention of ARF Prevention of ARF is much easier, is much easier,

more cost effective, more cost effective, and more and more

successful than its successful than its treatmenttreatmentFluid balance, proper medications, avoid Fluid balance, proper medications, avoid nephrotoxic drugs.nephrotoxic drugs.

‘‘Contrast material causes 10% of hospital Contrast material causes 10% of hospital acquired ARF’acquired ARF’

Hepatic DysfunctionHepatic Dysfunction

Primary Primary Secondary may be seen in ICU settingSecondary may be seen in ICU setting

Acute exacerbation of chronic liver diseaseAcute exacerbation of chronic liver disease

Jaundice, impaired synthetic activity-Jaundice, impaired synthetic activity-coagulation disorder, electrolyte imbalance, coagulation disorder, electrolyte imbalance, altered mental status-cerebral edema, renal altered mental status-cerebral edema, renal and pulmonary dysfunction, hepatorenal and pulmonary dysfunction, hepatorenal syndrome, ascites-spontaneous bacterial syndrome, ascites-spontaneous bacterial peritonitis, multi-organ failure. peritonitis, multi-organ failure.

Hepatic Dysfunction - Hepatic Dysfunction - ManagementManagement

Reversal of precipitating factorsReversal of precipitating factors Removal of offending drugsRemoval of offending drugs Correcting fluid/electrolyte Correcting fluid/electrolyte

abnormalitiesabnormalities Treating infectionsTreating infections Ammonia elimination by administering Ammonia elimination by administering

lactulose and/or neomycin.lactulose and/or neomycin. Adequate nutrition (sodium/protein Adequate nutrition (sodium/protein

restriction)restriction) Address coagulopathyAddress coagulopathy

Hepatorenal SyndromeHepatorenal Syndrome Renal dysfunction seen in approx. 40% of Renal dysfunction seen in approx. 40% of

patients in fulminant hepatic failurepatients in fulminant hepatic failure Mechanisms seems to be related to renal Mechanisms seems to be related to renal

vasoconstrictionvasoconstriction Characterized by azotemia, oliguria, low Characterized by azotemia, oliguria, low

urinary sodium (<10mEq/L) and high urinary sodium (<10mEq/L) and high urine osmolalityurine osmolality

Poor prognosis – improvements seen Poor prognosis – improvements seen using terlipressin (vasopressin analogue)using terlipressin (vasopressin analogue)

Kidneys not permanently damaged. Kidneys not permanently damaged.