Download surgical critical care

SURGICAL CRITICAL
CARE
Gastrointestinal System
Acute Renal Failure
Hepatic Dysfunction
Gastrointestinal System
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Stress Gastritis
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Abdominal Compartment Syndrome
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Nutritional Support
Pathophysiology of Stress Gastritis
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Hypovolemia
Decreased Cardiac Output
Splanchnic hypoperfusion
Acid back-diffusion, bicarbonate hyposecretion,
decreased mucosal blood flow and depressed
gastric motility…
Mucosal Erosion
Stress Gastritis / Gastric Ulceration
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Risk factors
Mechanical ventilation > 48hrs
 Coagulopathy
 Significant Burns
 Head Injury / Brain Insult
 Organ Transplantation / Immunosuppression
 High dose steroids
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Major Surgery, pancreatitis, renal failure, hepatic failure, multiple
traumatic injuries.
Prophylaxis
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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 ________.
Abdominal Compartment Syndrome
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‘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
Abdominal Compartment Syndrome
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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
Abdominal Compartment Syndrome
Bladder pressure accepted as subjective
approximation to intra-abdominal pressure
Grade
I
II
III
IV
Intra-abdominal pressure
10-14 mmhg
15-24 mmhg
25-35 mmhg
> 35 mmhg
Treatment
Resusc.
Resusc.
Decompression
Emergent re-exploration
Nutritional Support
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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.
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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)
Nutrition
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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.
Nutrition
How much to give? 2000-2500 kcal/day
Basal energy expenditure (kcal/day)
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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
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Multiply by ‘Stress factor’ approx. 1.5
2.5g protein/kg/day (1g normal)
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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
Acute Renal Failure
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High mortality >50% in the ICU setting
Classification
Prerenal
 Renal
 Post Renal
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First signs are oliguria (<400cc/24hrs) and rise in
creatinine levels. ( 30-40% of ARF is non-oliguric)
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
Example
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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.
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
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‘pigment deposition, retrograde pressure/tubular blockage, luminal edema’
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Alterations in ARF
 Metabolic acidosis
 Hyperkalemia
 Hyperphophatemia
 Hypocalcemia
 Hyponatremia
 Hypermagnesemia
Acute Renal Failure
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High mortality
Prolonged recovery course
Complication of renal replacement therapy
PREVENTION
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
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ARF – measurements & calculations
Prerenal Azotemia Tubular Injury
Urine Osmolality
> 500
< 350
U/P Osmolality
>1.25
<1.1
U/P creatinine
> 40
< 20
U/P urea
>8
<3
Urine sodium
<20
>40
FE Na
<1
>3
Fractional Excretion of Sodium
FE Na = excreted Na / filtered Na
FE Na = UNa/PNa x Pcreat / Ucreat
ARF - Treatment
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Fluid management
Correct electrolytes
Diuretics
Renal Replacement Therapy
Hemodialysis
 Continuous Venovenous Hemodialysis
 Continuous Arteriovenous Hemodialsys
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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’
Hepatic Dysfunction
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Primary
Secondary may be seen in ICU setting
Acute exacerbation of chronic liver disease
Jaundice, impaired synthetic activity-coagulation
disorder, electrolyte imbalance, altered mental statuscerebral edema, renal and pulmonary dysfunction,
hepatorenal syndrome, ascites-spontaneous bacterial
peritonitis, multi-organ failure.
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Hepatic Dysfunction - Management
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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
Hepatorenal Syndrome
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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.