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  1. Acute onset
  2. Bilateral infiltrates on chest radiograph
  3. Pulmonary artery wedge pressure < 18 mmHg (obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left ventricular failure suffices
  4. if PaO2:FiO2 < 300 mmHg acute lung injury (ALI) is considered to be present
  5. if PaO2:FiO2 < 200 mmHg acute respiratory distress syndrome (ARDS) is considered to be present

Patient Presentation And Diagnosis

  1. ARDS can occur within 24 to 48 hours of an injury or attack of acute illness. In such a case the patient.
  2. Usually presents with shortness of breath, tachypnea, and symptoms related to the underlying cause.
  3. ARDS is classically associated with hypoxemia, petechiae in the axillae and neurologic abnomalities such as mental confusion.
  4. Plain Chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of cases.


  1. ARDS is characterized by a diffuse inflammation of lung parenchyma.
  2. The triggering insult to the parenchyma usually results in an initial release of cytokines and other inflammatory mediators, secreted by local epithelial and endothelial cells.
  3. Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung parynchema and contribute in the amplification of the phenomenon.
  4. Typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls.
  5. The result is a critical illness in which the ‘endothelial disease’ of severe sepsis/SIRS is worsened by the pulmonary dysfunction, which further impairs oxygen delivery.


  1. Acute respiratory distress syndrome is usually treated with mechanical ventilation in the ICU.
  2. Treatment of the underlying cause
  3. Appropriate antibiotic therapy.
  4. Mechanical ventilation

Pressure Regulated Volume Control

  1. The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application.
  2. Low tidal volume ventilation was the primary independent variable associated with reduced mortality.
  3. APRV (Airway Pressure Release Ventilation) and ARDS/ALI
  4. Although a particular ventilation mode has yet to be “proven in clinical trials”* more effective than others in treating patients with ARDS.
  5. Positive End-Expiratory Pressure
  6. Positive end-expiratory pressure (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.
  7. Prone Position
  8. Distribution of lung infiltrates in acute respiratory distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion.
    1. Fluid Management
      Several studies have shown that pulmonary function and outcome are better in patients that lost weight or wedge pressure was lowered by diuresis or fluid restriction.
    2. Corticosteroids
      Significant improvement in ARDS using modest doses of corticosteroids.
    3. Nitric Oxide
      Inhaled nitric oxide (NO) potentially acts as selective pulmonary vasodilator.
    4. Surfactant Therapy
      To date no prospective controlled clinical trial has shown a significant mortality benefit of exogenous surfactant in ARDS.


  1. Pulmonary: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP).
  2. Gastrointestinal: hemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation.
  3. Cardiac: arrhythmias, myocardial dysfunction.
  4. Renal: acute renal failure (ARF), positive fluid balance.
  5. Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube.
  6. Nutritional: malnutrition (catabolic state), electrolyte deficiency.
  7. The mortality rate varies from 30% to 60%

Timing of nutritional support

  • Previously good nutritional status and moderately severe catabolic state:
    Less than 60 yrs - 14 days
    60-70 yrs - 10 days
    ≥ 70 yrs - 7 days
  • Nutritional support should be started before effects of starvation appear.
  • Routes of feeding- Enteral nutrition and Parenteral nutrition

Enteral nutrition

  1. The bowel works, use it.
  2. More physiologic, safe and less expensive.
  3. Preserves gut integrity, barrier and immune function.
  4. Supplies gut preferred fuels (glutamine, glutamate and short chain fatty acids), unlike standard PN.
  5. Prevents cholelithiasis by stimulating GB motility.
    Recommendation: Initiation within 24-48 hrs of ICU admission in hemodynamically stable pts

Contraindications of Enteral nutrition

  1. GI causes: severe diarrhoea, paralytic ileus, intestinal obstruction, severe GI bleeding, acute pancreatitis and high output external fistula.
  2. Cardiac causes: haemodynamic instability, low cardiac output, circulatory shock. Potential risk of GI ischemia.
  3. Lack of access: unobtainable safe access to GIT.
  4. Complications of enteral feeding: aspiration, severe diarrhoea and intestinal ischemia or infarct.

Routes of enteral nutrition

  1. Nasogastric tube
  2. Naso duodenostomy tube
  3. Nasojejunal tube - ESPEN guidelines: Jejunal feeding is likely to be the best
  4. Percutaneous feeding gastrostomy
  5. Jejunostomy tub

Complications of enteral feeding

  1. Gastric retention, vomiting and aspiration: more often with gastric feeding. Incidence varies from 1-44 %.
  2. Mechanical problems:
  3. Feeding tube obstruction (10%)- flush the tube with water before and after infusion of nutrients.
    If tube blocked and can’t be flushed with water-›
  4. Flush tube with warm solution of 7.5% sodium bicarbonate.
  5. If unsuccessful, replace the feeding tube.
  6. Malposition: assoc. with blind bedside tube placement. Contributing factors: Altered mental status due to injury or sedation, absence of gag reflex, inability to cough, dysphagia or endotracheal intubation
  7. Tube position in the GIT should be confirmed. (Various methods: Radiographic, assessment of myoelectric activity, aspiration of gastric contents or aspiration of bile and Direct laryngoscopy).
  8. Diarrhoea: most troublesome complication
  9. Steps to control diarrhoea:
  10. Reduce the feeds by half, avoid lactose and bolus feeding.
  11. Use pectin and kaolin combination and aluminium hydroxide.
  12. Use isotonic solution.
  13. Stop any diarrhoea causing antibiotics and magnesium antacids.
  14. Special feeding formulas containing amino acids or small peptides may be used.

Parenteral nutrition

Pharmacological therapies where nutrients, vitamins, electrolytes and medications are delivered via venous route to those patients whose GIT is not functioning and are unable to tolerate enteral nutrition.
Indications of parenteral nutrition
  • General indications
    Inadequate oral or enteral nutrition for atleast 7-10 days (ASPEN and CCPG).
    ESPEN: initiate within 24-48 hrs of ICU pts who can’t be fed enterally
    • Pre existing severe malnutrition with inadequate oral or enteral nutrition.
      Anticipated or actual inadequate oral or enteral intake
    • Conditions that impair absorption of nutrients:
      Enterocutaneous fistula
      Small bowel obstruction
  • Effects of radiation or chemotherapy
    • Need for bowel rest:
      Severe pancreatitis
      Inflammatory bowel disease
      Short bowel syndrome
      Ischemic bowel Peritonitis
      Pre and post op status
    • Motility disorders: Prolonged ileus
    • Haemodynamic instability
    • Massive GI bleeding
    • Unacceptable aspiration risk
    • Hyperemesis gravidarum, eating disorders
    • Significant multiorgan system disease
Complications of parenteral nutrition
  Mechanical Metabolic/GI Infections
First 48 hrs. Malposition, Haemothorax, Pneumothorax, Air embolism, Blood loss, Puncture of Subclavian/ Carotid Art. Fluid overload, Hypoglycemia, Hypophosphatemia, Hypokalemia, Hypomagnesemia, Refeeding syndrome _ _
First 2 weeks Catheter displacement, Thrombosis, occlusion, Air embolism Hypoglycemic coma, Acid base and Electrolyte imbalance Catheter induced sepsis, Exit site infection
3 months onwards Tear of catheter, catheter thrombosis, Air embolism, blood loss Ess. FA def., Vitamins or trace element def, Metabolic bone ds., Liver ds. Tunnel infection, Catheter induced sepsis, Exit site infection

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