UMEM Educational Pearls - Critical Care

Critical Care Pearls for Traumatic Brain Injury

• Avoid hypotension and hypoxia - SBP < 90 and/or PaO2 < 60 are associated with significant increases in morbidity and mortality
• Hypertonic saline remains controversial - a recent large, controlled trial did not show any early or long-term benefit
• ICP monitoring routinely recommended in patients with GCS < 8 - they have a 60% chance of increased ICP
• Maintain ICP < 20 mmHg and CPP > 60
• Supportive care
  • Elevate the head of bed > 30 degrees, if possible
  • Control fever
  • Provide analgesia and sedation
• Ventilator management - keep PaCO2 between 30-35 mmHg
• Surgery - last resort to controlling increased ICP
  • Decompressive craniotomy
  • Decompressive laparotomy

• Binding of vasopressor agents to their receptors is influenced by pH (and temperature and concentration)
• Acidic conditions have been shown to alter receptor numbers on cell surfaces as well as alter binding affinity
• Overall, pH values > 7.15 do not have an appreciable clinical effects on vasopressors
• At pH values < 7.1 reductions in effectiveness become apparent
• Routine administration of bicarbonate remains controversial
• Aggressively search for and treat the underlying cause of the acidosis

 

Hyperammonemia in the Critically Ill

• Patients with acute hyperammonemia have significant morbidity and mortality 
• Fulminant hepatic failure is the most common cause of acute hyperammonemia in adult ICUs
• Other causes include TPN, GI hemorrhage, steroid use, trauma, multiple myeloma, infection with urease-splitting organisms, and drugs (salicylates, valproate) 
• Cerebral edema, intracranial hypertension, seizures, and herniation are the most significant effects
• Initial management should focus on treating intracranial hypertension - mannitol, hypothermia, N-acetylcysteine have been used
• Lactulose has not been shown to reduce mortality in acute hyperammonemia but is unlikely to be harmful

Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest 2007;132:1368-1378.

[RESENT - STILL FIXING CODE - THESE TEST EMAILS SHOULD CEASE SHORTLY... SORRY FOR THE INCONVENIENCE]

• Abdominal compartment syndrome (ACS) is increasingly identified in the critically ill medical patient population
• ACS is defined as a sustained intra-abdominal pressure > 20 mmHg associated with new organ dysfunction
• Primary organs adversely affected by ACS include cardiac, pulmonary, GI, and renal
• To date, associated mortality rates have ranged from 27% to 50%
• Risk factors for ACS include:
  • massive fluid resuscitation ( >10 L crystalloid in 24 hours)
  • massive transfusion ( > 10 U PRBCs in 24 hours)
  • severe sepsis or septic shock from any cause
  • mechanical ventilation
  • PEEP > 10 cm H20
• Intravesicular (bladder) pressures are currently the standard monitoring modality
• Decompressive laparotomy is the current standard for management of ACS

DIC is the simultaneous occurrence of widespread (micro) vascular thrombosis, leading to compromised blood supply to vital organs Although major bleeding can be seen in some, the more common complication of DIC is organ failure DIC is not a disease itself but secondary to an underlying disorder Sepsis, solid and hematologic malignancies, severe trauma, and obstetrical emergencies (amniotic fluid embolism, abruption) are the most common disorders associated with DIC A prospectively validated scoring system (Toh CH, et al. J Thromb Haemost 2007;5:604-6.) is used for diagnosis and is comprised of platelet count, fibrin split products, PT, and fibrinogen level The key to treating DIC is vigorous treatment of the underlying disorder Platelet transfusion is generally only given for patients with major bleeding (i.e. intracranial) with platelets counts < 50 k

-Reexpansion pulmonary edema represents a potentially life-threatening complication of tube thoracostomy (mortality rate as high as 20 percent) -It usually occurs after rapid reexpansion of a collapsed lung in patients with a pneumothorax -It may also follow evacuation of large volumes of pleural fluid (>1.0 to 1.5 liters) or after removal of an obstructing tumor -The incidence of edema appears to be related to the rapidity of lung reexpansion and to the severity and duration of lung collapse -The clinical manifestations vary from isolated radiographic changes to complete cardiopulmonary collapse -Treatment is supportive, mainly consisting of supplemental oxygen and, if necessary, mechanical ventilation

-Non-invasive ventilation (NIV) is a form of ventilatory support that avoids intubation. -NIV refers to the provision of inspiratory pressure support + PEEP via a nasal or face mask (BiPAP, CPAP). -Strong evidence from randomized trials supports NIV to avoid intubation in patients with acute respiratory failure secondary to COPD exacerbation, acute cardiogenic pulmonary edema, and in immunocompromised patients (AIDS, transplant). -NIV can be considered in asthma exacerbations, pneumonia, and ARDS however the supporting evidence for these conditions is fairly weak. -Contraindications for NIV include respiratory arrest, hemodynamically unstable, unable to protect the airway, excessive secretions, uncooperative/agitated, and recent UGI or airway surgery. -You should expect to see clinical improvement within 1 to 2 hours.

-Phosphate is predominantly an intracellular ion that is critical for an array of cellular processes -Hypophosphatemia is most commonly seen in alcoholics, DKA, and sepsis: frequency rates of 40%-80% -Severe hypophosphatemia ( < 1.0 mg/dL) in the critically ill can manifest as widespread organ dysfunction: respiratory failure (diaphragmatic weakness), CHF (decreased myocardial contractility), rhabdomyolysis, arrhythmias, seizures, hemolysis, impaired hepatic function, and depressed WBC function -Severe hypophosphatemia should be treated with intravenous replacement: 0.08 - 0.16 mmol/kg over 2-6 hours -Be aware of complications from too rapid intravenous replacement: hypocalcemia, tetany, hypotension, volume excess, and metabolic acidosis

-Norepinephrine: has both alpha-1 and beta-1 activity; stronger alpha than beta receptor agonist; increases MAP primarily through increase in SVR; dose 2-20mcg/minute -Phenylephrine: all alpha-1 activity; increases MAP through increase in SVR; initial dose 100-180 mcg/minute and titrate 40-60 mcg/min; primarily a 3rd line vasopressor -Vasopressin: a non-adrenergic vasoconstricting agent; activates vasopressin receptors; dose 0.01-0.04 Units/min; currently used as a second-line agent in the setting of sepsis; should not be used as the sole vasopressor medication due to gut and cardiac ischemia -Dopamine: activates dopaminergic receptors; at doses of 10-20 mcg/kg/min it has both alpha-1 and beta-1 activity; increases MAP primarily through increases in CO; stronger chronotropic agent than norepinephrine - will worsen existing tachycardia -Epinephrine: has potent beta-1 activity with moderate alpha-1 and beta-2 activity; at lower doses increases MAP through increase in CO; at higher doses increases MAP by increase in SVR; primarily used in anaphylactic shock; dose 1-20 mcg/min

-Epinephrine is the drug of choice for anaphylaxis -Several studies indicate that epi is underutilized in ED patients with anaphylaxis -Indications for epinephrine include bronchospasm, laryngeal edema (hoarseness, stridor, difficulty swallowing), hypotension, rapidly progressive reaction, and severe gastrointestinal symptoms (due to bowel edema) -The dose of epinephrine is 0.3 to 0.5 mL of 1:1000 IM -Pearl: IM injection into the lateral thigh (vastus lateralis) has been shown to produce considerably faster time to maximum drug concentration than subq injection or IM injection into the deltoid

-Think about acalculous cholecystitis in the critically ill patient with fever, abdominal pain, and elevation of LFTs and bilirubin -Pathophys thought to be due to SIRS, biliary stasis, and ischemia -Abdominal pain is not always in the right upper quadrant -Patients have a high rate of complications - gangrene or perforation (40% to 60%) -Diagnostic studies: ultrasound (sens. 70%), HIDA (sens. 80% to 90%), CT (sens. 90%) -Consult surgery early because treatment of choice is surgical cholecystectomy; some can be treated with percutaneous cholecystostomy but this is up to your consultant

-Post-intubation hypotension can occur in a substantial proportion of patients -Before attributing this to the effects of your sedative medications, you must think about pnemothorax, hyperinflation from overzealous bag-valve mask ventilation, and hypovolemia -Pneumothorax - auscultate the lungs and repeat the CXR -Hyperinflation - disconnect the patient from the ventilator and allow them to "deflate" -Hypovolemia - give a fluid bolus

-When setting the ventilator, many of us use an initial tidal volume of 6 ml/kg -This number comes from ARDSnet data that demonstrated improved mortality with low tidal volumes in patients with ARDS/ALI -It is important to note that your calculation of 6 ml/kg is based upon IDEAL BODY WEIGHT (not total body weight) -For males: IBW = 50 kg + 2.3 kg for each inch over 5 feet. -For females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.

-Remember that oxgenation is affected by changes in PEEP and/or FiO2 -For changes needed in ventilation (pH and pCO2), you alter the respiratory rate (RR) and/or tidal volume (TV) -Changes in RR produce a greater effect on pH and pCO2 than changes in TV -Focus more on maintaining a pH between 7.3 - 7.4, rather than on returning pCO2 to normal

-One of the most common reasons for intubation/mechanical ventilation in the ED is patient fatigue -Essentially, patients are unable to keep up with the work of breathing -Patient work of breathing can be significant in CPAP, SIMV, and Pressure Support modes of mechanical ventilation -Avoid these as initial modes if your patient has respiratory fatigue

Mechanical Ventilation "Knobology" - Oxygenation -FiO2 and PEEP are used to improve oxygenation in the ventilated patient -Immediately following intubation, start with an FiO2 of 100% -Increase PEEP by 2-3 cm H2O every 10-15 minutes to achieve the desired saturation -As you titrate PEEP, have respiratory therapy provide you with plateau pressures (maintain Pplat < 30) Mike

TRALI - Transfusion Related Acute Lung Injury * TRALI has now emerged as the primary cause of transfusion-associated mortality, surpassing infectious complications and ABO mismatch * TRALI is defined as new ALI in a patient receiving, or having just received (within the past 6 hours), a blood product transfusion * All plasma-containing products have been implicated (FFP and platelets are the top offenders) * Clinically, patients present with dyspnea, tachypnea, and hypoxia * CXR findings are consistent with noncardiogenic pulmonary edema * There is no unique treatment for TRALI; most patients have resolution within 96 hours * AVOID diuretics as these patients are often volume depleted Reference: 1. Looney MR. Newly recognized causes of acute lung injury: transfusion of blood products, severe acute respiratory syndrome, and avian influenza. Clin Chest Med 2006;27:591-600.

Make sure the Cordis is the right size when floating a pacing wire * At some point in your career, you may need to "float" a transvenous pacing wire * When inserting the wire, you need to make sure you have the right size Cordis * In general, a pacing wire should be inserted through a 6F Cordis (0.198 mm) * Many introducer kits have a 7.5F Cordis (0.2475mm) that is used for insertion of a PAC * Blood loss, infection, and air embolism are risks that can occur when the Cordis catheter used is too large Reference: 1. Marcucci L, ed. Avoiding common ICU errors. Philadelphia; Lippincott Williams & Wilkins; 2007:275-6.

Critical Illness Neuromyopathy (CINM) * CINM is the most common peripheral neuromuscular disorder encountered in the ICU * CINM may contribute to delayed weaning and prolonged ventilation * Risk factors for CINM include SIRS/MODS, sepsis, and hyperglycemia (corticosteroid use still controversial) * Current mainstay of management is directed at prevention * EM take home point -> Judicious use of medications associated with the development of CINM (aminoglycosides, neuromuscular blocking agents) Reference: De Jonghe B, Lacherade JC, Durand MC, et al. Critical illness neuromuscular syndromes. Crit Care Clin 2007;23:55-69. (compliments of Dr. Winters)

Fungal Infections * Fungal isolates are an increasingly common source of bloodstream infections in critically ill patients * Mortality ranges from 20% to 60% in some series * 50% are non-albicans species (C.glabrata, C.parapsilosis, C.tropicalis, and C. krusei) * Risk factors include ventilated patients, TPN, high APACHE scores, abdominal surgery, and prolonged ICU stays * Think of fungal infections in the septic patient with hypothermia and bradycardia * Newer antifungal agents such as voriconazole and caspofungin have improved efficacy against n