Acute Liver Failure

• Acute liver failure (ALF) is defined as the onset of encephalopathy and coagulopathy within 26 weeks of jaundice in a patient without prior history of liver disease
• ALF has an extremely high mortality
• The most common cause of ALF include Tylenol, HSV, autoimmune hepatitis, HBV, and acute fatty liver of pregnancy/HELLP
• Complications EPs are likely to see/manage include hepatic encephalopathy, infection, circulatory dysfunction, bleeding, and seizures
• Fungal infections may be present in one-third of patients with ALF (Candida)
• Non-convulsive seizure activity occurs in a high proportion of patients with ALF and encephalopathy - consider EEG for severly encephalopathic patients and those with a sudden deterioration in neuro status

Stravitz RT, et al. Intensive care of patients with acute liver failure. Crit Care Med 2007;35:2498-2508.

A few days ago Dr. Jump and I had a case of an acute variceal hemorrhage.  Dr. Bond already sent out a great pearl earlier in the year highlighting the importance of octreotide in acute variceal bleeding.  In fact, octreotide alone can result in cessation of hemorrhage in up to 80% of patients.  To add onto Dr. Bond's pearl:

• Don't forget about antibiotics in acute variceal hemorrhage
• These patients have a relatively high incidence of bacteremia, which leads to worse outcomes
• Antibiotics have been shown to decrease infection rates and are associated with decreased rebleeding and the need for transfusions
• A 3rd generation cephalosporin is currently the recommended antibiotic of choice

• Acute chest syndrome (ACS) is the leading cause of death in sickle cell patients
• ACS is defined by the presence of a new infiltrate and one of the following: chest pain, wheezing, fever, tachypnea, or cough
• Early and aggressive therapy is needed to minimize mortality
• Up to 50% of patients develop respiratory failure
• Treatment
  • Broad spectrum antibiotics - including a macrolide
  • Pain control to reduce hypoventilation
  • Early use of blood transfusion to improve O2 carrying capacity
  • Incentive spirometry
  • Bronchodilators if wheezing present
  • Hematology consult

 

• It is traditionally taught that in hypotensive patients the presence of a carotid pulse corresponds to a SBP of 60-70 mmHg, a femoral pulse with a SBP of 70-80 mmHg, and a radial pulse with an SBP of at least 80 mmHg
• These physical exam estimates of BP have been shown to poorly correlate with the patient's actual BP
• Similarly, non-invasive measurements of BP (automated cuff) in patients with hypotension may either overestimate or underestimate SBP by as much as 20 mmHg
• Since physical exam estimates and non-invasive measurements are inaccurate in low-flow states, utilize invasive arterial monitoring
• Radial and femoral artery sites have been found to produce results that are clinically interchangeable

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

Important EM pearls from the recent 2007 IDSA/ATS guidelines for treatment of community-acquired pneumonia (CAP) Patients should be treated for a minimum of 5 days CURB-65 a new pneumonic; any patient with ? 2 warrants admission Confusion Uremia elevated Respiratory rate low Blood pressure age > 65 Outpatient CAP treatment Healthy + no abx in past 3 months ? macrolide Comorbidities OR use of abx within last 3 months ? a respiratory fluoroquinolone OR ?-lactam + macrolide Inpatient CAP treatment ICU patients ? ?-lactam + either azithromycin or a respiratory fluoroquinolone Non-ICU patients ? respiratory fluoroquinolone OR ?-lactam + macrolide Mandell LA, et al. Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults Clinical Infectious Diseases 2007;44:S27-S72

-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