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.
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