evaluating the patient’s clinical status.
Hemoglobin 8–10 g/dL: transfusion generally not indicated, but considered for some (e.g. symptomatic anemia, bleeding, acute coronary syndrome with ischemia, and hematology/oncology patients with severe thrombocytopenia who are at risk of bleeding).
Hemoglobin >10 g/dL: transfusion generally not indicated except in exceptional circumstances.
Critically ill patients pose an increased risk of developing venous thromboembolism (VTE) due to their increased length of hospitalization, inactivity, immobilization, and often hypercoagulable states. Mortality associated with deep venous thrombosis is significantly high and often progresses to more serious complications such as pulmonary embolism.
Prophylaxis for VTE should be considered in all patients and initiated at the time of admission. The majority of ICU patients fall under the high risk criteria for developing VTE and pulmonary embolism, particularly those patients who have had an operation or have had major trauma. These patients should be initiated on prophylaxis with low dose unfractionated heparin (5000 U SC every 12 hours) or low molecular weight heparin (enxaparin 40 mg SC every day) as soon as possible, if not contraindicated by bleeding or coagulopathy. Intermittent pneumatic compression devices should be provided to all patients until anticoagulants can be safely initiated.
Gastrointestinal complications
Critical illness is associated with a severe catabolic stress state which contributes to the risk of infections, increased length of hospitalization, and mortality. The Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition now recommend early enteral nutrition initiated between 24 and 48 hours of admission.
Enteral nutrition increases blood flow to the GI tract, decreases bacterial translocation, improves immune‐mediated response in sepsis, and improves overall survival.
There have been numerous prospective randomized trials performed in the critically ill comparing the effects of enteral versus parenteral nutrition. These trials showed that parenteral nutrition had a higher number of complications associated with infections (particularly pneumonia and central line infections), while enteral nutrition had a significant reduction in hospital LOS, cost of nutrition therapy, and infection rates.
Critically ill patients have a higher risk of developing stress‐related GI lesions due to hypoperfusion of the gastric mucosa, reduction in the protective factors of the mucosa, and increase in gastric acid secretion. These lesions may result in upper GI bleeding which is associated with an increased risk of death in the ICU.
In a large, prospective, multicenter trial of 2252 ICU patients by Cook et al., the mortality of patients with stress ulcer bleeding was 49% versus 9% in those with stress ulcers, but without an episode of GI bleeding. It also identified mechanical ventilation and coagulopathy as the two main risk factors associated with stress ulcer‐related bleeding.
Acid suppressive medications effectively decrease bleeding rates and are therefore recommended as prophylaxis in high risk patients. Proton pump inhibitors and histamine 2 receptor antagonists have been shown to prevent GI bleeding in the critically ill and are recommended in ICU patients with high risk such as those on mechanical ventilation, or with sepsis or septic shock, coagulopathy, and a history of upper GI bleeding in the past 12 months.
The routine use of stress ulcer prophylaxis does not reduce overall ICU mortality and therefore the need for stress ulcer prophylaxis should be re‐evaluated once the critical period has passed.
Renal complications
Hyponatremia remains one of the most common electrolyte disorders in the critically ill due to both excess fluid administration as well as impaired renal handling of fluids. Hyponatremia is a predictor of increased mortality in congestive heart failure and a marker of severity of illness in the general patient population. Daily monitoring of intravenous fluids and avoiding hypotonic solutions are key in preventing this electrolyte abnormality.
Central pontine myelinolysis (CPM) is an osmolar disruption in the brain that results in non‐inflammatory demyelination especially in the pons. CPM is a life‐threatening complication of rapid correction of hyponatremia. A conservative approach should be taken to correct hyponatremia by no more than 8 mEq/L over the first 24 hours, and no more than 15–20 mEq/L over 48 hours. Monitoring serum sodium frequently is crucial to the prevention of unrecognized rapid correction; when 3% saline is used, sodium should be monitored every 4 hours.
Hyperkalemia can result from renal insufficiency, rhabdomyolysis, burns, and/or trauma. It is also associated with commonly used medications such as digoxin, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, heparin, NSAIDs, and succinylcholine. Treatment of hyperkalemia includes insulin plus dextrose, inhaled high dose beta‐agonist; calcium is administered in the setting of electrocardiography changes such as peaked T waves. Sodium polystyrene sulfate is another agent often used for treatment of hyperkalemia, however it should be noted that it has a very slow onset of action and has been linked to a complication of bowel necrosis.
Contrast‐induced nephropathy (CIN) is a common cause of hospital‐acquired acute kidney injury in the ICU. It leads to prolonged hospital stay, adverse clinical outcomes, and a 5.5% increased overall mortality. Critically ill patients are at a higher risk of developing CIN due to their greater severity of illness and comorbid conditions such as sepsis, hypotension, hypovolemia, and concomitant use of nephrotoxic agents. The mainstays for CIN prevention are hydration (pre‐ and post‐contrast) and the use of low osmolality contrast agents.N‐acetylcysteine (NAC) has been theorized as a potential agent in preventing CIN. Recent trials have looked at the efficacy of NAC in preventing CIN in the ICU by comparing the incidence of acute renal impairment after administration of iodinated contrast with or without NAC treatment. The results suggest that NAC impedes the rise of serum creatinine but does not improve overall renal function. Additionally, NAC carries a risk of adverse side effects such as anaphylactoid reactions when administered intravenously. Its utility remains questionable and is therefore not recommended for the prevention of CIN.
Procedure‐related complications
Central venous catheterization (see Chapter 3) is a commonly performed procedure in the ICU. Complications vary with site and number of attempts at cannulation. They can be divided between infectious complications and mechanical complications such as arterial puncture, pneumothorax, and atrial/ventricular arrhythmias. Higher rates of infections have been reported with femoral sites versus either subclavian or internal jugular sites while the subclavian site has been associated with difficult to control bleeding.
Ultrasound‐guided catheter placement has shown clear evidence in reducing the rate of the above mentioned mechanical complications. We recommend the use of ultrasound‐guided central line placement whenever possible, including wire visualization by ultrasound prior to cannulation. A quick point‐of‐care ultrasound of the lungs can also be performed post‐procedure to assess for a pneumothorax. Telemonitoring should occur throughout the procedure for detection of premature ventricular complexes, particularly while introducing the guidewire and to monitor BP and oxygenation.
Endotracheal intubation (see Chapter 1) is a commonly performed procedure in the ICU. Circulatory collapse remains the most common and highest risk complication during the peri‐ and post‐intubation period, followed by hypoxia and aspiration. Unlike intubation performed
