Abdominal problems in ICU

AHA/ACS
Intra abdominal hypertension

abdominal compartment
syndrome
Risk factors for IAH

1. High BMI
2. Abdominal surgery
3. Ascites,
4. Hypotension/vasoactive therapy,
5. Respiratory failure
6. Excessive positive fluid balance
Indications for IAP measurements
1. Obesity
2. Sepsis with capillary leak
3. Severe burns.
4. Severe acute pancreatitis
5. Large volume fluid resuscitation
6. Ruptured aortic aneurysms
7. Abdominal trauma (especially if acidosis, hypothermia
and coagulopathy)
8. Abdominal surgery
9. Bowel paralysis
10. Liver failure with ascites
Management of IAH/IAP
1. Reduce or hold Enteral Nutrition
2. Decompress luminal contents-NG aspiration,
Prokinetics and rectal enemas, colonoscopy
3. Decompress peritoneal cavity-drainage /Sx
4. Target negative balance
5. Adequate analgesia+sedation ± muscle relaxation
Acute Mesenteric ischaemia
Occlusive Non-occlusive

Non-occlusive mesenteric ischaemia (NOMI),

Venous related to systemic hypoperfusion.
Arterial-
thrombosis
• Postoperative with
Risk previous h/o AMI
• Abdominal vascular
Embolism factors surgery, especially after
ruptured AAA
• Bowel obstruction
: • High-dose vasopressors.

Thrombosis
 Acute Mesenteric ischaemia
How will you suspect?

Abdominal signs
• Pain, abdominal
distention
• Feeding intolerance,
bowel paralysis
• Diarrhoea, melaena
Laboratory markers
• Metabolic acidosis not explainable by
other reasons
• Increased lactate values
• Increase of inflammatory markers
not explainable by other reasons.
Acute Mesenteric ischaemia
How will you confirm
diagnosis?
CT angiography
Acute Mesenteric ischaemia
Patient in septic shock with
NOMI-non occlusive high dose vasopressors
Acute colonic pseudo obstruction (Ogilvie’s syndrome)

Megacolon
 Acute colonic pseudo obstruction (Ogilvie’s syndrome)

Management
• Exclude mechanical bowel obstruction
• Avoid oral osmotic or stimulant laxatives.
• Avoid and minimize opioids and anticholinergic
medications
• Nasogastric (and rectal) tubes for decompression
• Fluids and electrolytes correction
Acute colonic pseudo obstruction (Ogilvie’s syndrome)

Drug Treatment-Neostigmine
Acute colonic pseudo obstruction (Ogilvie’s syndrome)

Drug Treatment-Neostigmine

if neostigmine is contraindicated or ineffective

Endoscopy may be considered

Acute colonic pseudo obstruction (Ogilvie’s syndrome)

Drug Treatment-Neostigmine

if neostigmine is contraindicated or ineffective

Endoscopy may be considered

Failed

Surgery
Clostridium difficile colitis and toxic megacolon

• Nosocomial diarrhoea
• Major cause: antibiotic exposure and cross contamination
• PPI: major risk factor
• Two toxins: A (leak toxin), B (inflammatory)
Clostridium difficile colitis and toxic megacolon

Diagnosis- A two-step approach:

Step 1. Screen using GDH (detects

Step 2. Perform an EIA for
all C. difficile strains including non-
toxin.
toxigenic/non-pathogenic strains).
 Clostridium difficile colitis and toxic megacolon

Radiography-CT

1. Neither sensitive nor specific

2. Colonic wall thickening
3. Low-attenuation mural thickening
4. Pericolonic fat stranding
5. Colonic dilatation >6 cm in severe
cases
Clostridium difficile colitis and toxic megacolon
If Lab diagnosis-inconclusive
Go for endoscopy

1. Direct visualization of
pseudomembranes
2. Raised, yellowish white, 2- to 10-mm
plaques on an erythematous
andoedematous mucosa.

Pseudomembraneous colitis may be caused by other organisms such as Salmonella.

 Clostridium difficile colitis and toxic megacolon
Management:
General
1. Minimize antibiotics exposure
2. Fluid and electrolytes
replacement
3. Avoid anti-motility medications
4. Minimize PPI use
5. Contact precautions to prevent
transmission
6. Measurements of intra-
abdominal pressures.
Medications
Mild-to-moderate disease:
Oral Metronidazole +Oral vancomycin
Severe or complicated CDI:
Oral vancomycin, +Metronidazole i.v.
Fidaxomicin if poor response to oral vancomycin.
Surgery
Early surgical consultation if presence of peritoneal signs,
severe ileus, and toxic megacolon
Total colectomy may be indicated in most severe rare
cases.
Presence of abdominal problems is not always a reason to
delay EN. In the majority of critically ill patients, EN can be
initiated at a low rate with close monitoring of tolerance.