Pathway 1: Altered Level of Consciousness
(Adult and Pediatric)
The team continues the resuscitation along the pathway suggested by the initial clinical impression. Each pathway includes a complete, thorough, and rapid physical examination with additional history taking. The team leader is wary of conditions that may not be apparent. To obtain additional clinical data or to correct a missed or newly developed condition, the team leader repeats the initial survey if the patient is not responding satisfactorily.
This section applies to situations of neurological impairment in which the cause and/or treatment are not immediately apparent. Many of the topics covered here may apply to confusion, delirium, coma, and/or seizures.
Clinical Consideration in Decreased Level of Consciousness/Coma/Delirium
The guiding memory phrase for diagnosing altered levels of consciousness is “DONT forget the TIPS from the vowels: AEIOU.”
The first step (after airway management and stabilization of life threats) is to assess for problems that may be immediately diagnosed and treated. DO the DONT: Dextrose, Oxygen, Narcan, and Thiamine.
Dextrose: Assess blood sugar by bedside testing or if not available, give 1 amp of D50 IV for presumed hypoglycemia. (See thiamine for precautions.) PEDS: child: 2 mL/kg D25; neonate: 2 to 4 mL/kg D10.
Oxygen: Clinical hypoxia is often apparent as an airway/breathing problem, but monitor O2 saturation whenever possible. Use liberally if O2 status is in doubt.
Narcan: Consider administering whenever narcotic intoxication cannot be ruled out. The dose is 0.4 to 2.0 mg IV every 2 to 3 min prn. PEDS: Initial dose is 0.01 mg/kg to 0.03 mg/kg; increase the dose to 0.1 mg/kg IV. Neonatal dose is 0.1 mg (0.25 mL of 0.4 mg/mL)/kg IV, IO, or ET. Problems with Narcan are usually minimal and rare but include precipitation of the withdrawal syndrome, which can include seizures in addicted neonates.
Thiamine: Administer this critical vitamin at a dose of 100 mg IV to patients who are debilitated or may be chronic alcoholics, preferably before giving D50 to adults.
A positive response to an intervention suggests which clinical direction to pursue. After completing the DONT sequence, if an altered level of consciousness (LOC) persists and its cause is still puzzling, continue through the rest of the mnemonic TIPS from the vowels: AEIOU. Review the list and start with the most likely condition given the patient’s circumstances.
ASSESSMENT AND MANAGEMENT
T — TRAUMA, TEMPERATURE, TUMOR
Traumatic Head Injury
Suspect
head trauma in all cases until this condition is ruled out or another
cause is identified, as the exam may or may not reveal signs of cranial
trauma. CT imaging is necessary to diagnose the different types of
intracerebral bleeding. PEDS:
Perform an
ophthalmoscopic examination of
the retinas in all infants with a decreased level of consciousness
(shaken baby syndrome). Keep the possibility of trauma in mind. Vol
I—Pathway 8 Adult Trauma, Pathway 9 Pediatric Trauma
Hypothermia
Vol III—ENV1 Hypothermia
Assess temperature in all patients under all conditions. Core temperature measures are needed for management of extreme cases. Note: many thermometers do not register temperatures lower than 90°F, so a low-reading rectal probe thermometer is needed if low body temperature is suspected. Categorize and treat hypothermia as follows:
Mild hypothermia (92°F to 95°F [33.3°C to 35°C]). A patient may be passively or externally rewarmed with blankets or forced-air, commercially available, plastic or paper blankets.
Moderate hypothermia (86°F to 92°F [30°C to 33.3°C]). A patient may be externally rewarmed if cardiovascular function is intact.
Severe hypothermia (below 86°F [30°C]). Patients with severe hypothermia are often in cardiac arrest or severe bradycardia and are at risk for decompensating to ventricular fibrillation. When monitoring is available, chest compressions are recommended only for ventricular fibrillation (VF) or asystole; avoid CPR if any organized rhythm is present, even if pulses are not palpable. Handle gently (VF is easily precipitated in a hypothermic patient) but manage airway as needed, including intubation. Make attempts to defibrillate to a maximum of three shocks. If these are unsuccessful, postpone further attempts until temperature is 86°F (30°C) or higher. Generally, avoid cardiac medications until the patient has been rewarmed; these medications don’t work at low temperatures and accumulate without being metabolized, causing problems when rewarming occurs. External rewarming may be hazardous in severe hypothermia.
Employ techniques of core rewarming. These include:
-
warmed IV fluids (40°C to 43°C [104°F to 109°F]); avoid volume overload
-
warm lavage of bladder (through Foley catheter) and stomach (through NG tube),
-
heated humidified O2 ventilation at 42°C to 46°C [108°F to 115°F] by mask,
-
warmed saline lavage of the mediastinum through chest tube (left side or bilateral),
-
peritoneal lavage with warm saline,
-
AV rewarming with femoral catheters and Level I (or other) blood warming circuit, or
-
complete AV bypass.
Hyperthermia
Fever is a physiologic response to many conditions, including
infection. Hyperthermia
is a pathological elevation in body temperature due to inability to
lose heat. Heat exhaustion is a fluid/electrolyte problem manifested by
symptoms such as weakness and fainting. Heat stroke is defined by
hyperthermia (usually > 104°F [40°C]) and change in mental
status.
Patients at risk for heat stroke are those exposed to heated
environments, young children and the geriatric population, and those
taking certain medications, especially phenothiazines.
Treatment of
heat stroke
Besides
the usual resuscitative measures, rapid cooling is required. This may
take the form of cold packs to axillae, neck, and inguinal areas; the
use of tepid water spraying and fans; or ice water immersion (which is
less recommended). Shivering interferes with cooling and may be treated
with benzodiazepines and/or phenothiazines (even though these drugs may
also predispose to hyperthermia).
Malignant hyperthermia is an uncommon but life-threatening disease seen with use of anesthetics, including drugs used for RSI. Malignant hyperthermia usually comes on dramatically after administration of a drug. (Monitor post-RSI patients who have a temperature.) Classic signs and symptoms include fever, rigidity, tachycardia, tachypnea, metabolic acidosis, or respiratory acidosis. Discontinue any inciting agent(s), institute cooling measures (Vol III—ENV2 Hyperthermia/Heat Stroke), check for acidosis regarding bicarbonate treatment (Vol III—END/M6 Acid Base), and give dantrolene 1 to 3 mg/kg IV; PEDS: 0.5 to 1 mg/kg IV. Search for end-organ damages resulting from this insult including respiratory failure, renal failure, DIC, cardiovascular collapse, or rhabdomyolosis.
Malignant hyperthermia may also be caused by various antipsychotics, which is called neuroleptic malignant syndrome. In addition to high temperatures, findings include labile blood pressure and muscular rigidity. To treat, initiate cooling measures, aggressive support care, muscle relaxation with either paralyzing agents (nondepolarizing neuromuscular blocking agents,(Vol III—AIR1 Rapid Sequence Intubation) or non-paralytic agents such as dantrolene 1 to 3 mg/kg IV (PEDS: 0.5 to 1 mg/kg IV). Consider adding bromocriptine 2.5 to 10 mg PO. Again, for more information, see Vol III—ENV2 Hyperthermia/Heat Stroke.
Tumor of the Brain
If
brain tumor (either primary or metastatic) is suspected, obtain a head
CT for diagnosis. Contrast may be needed for definition of a mass.
Steroids (Decadron 10 to 20 mg IV/IM. PEDS: 0.25 to 0.5 mg/kg IV)
may
be dramatically helpful in reducing edema and its mass effect.
I — INFECTION
Meningitis/Encephalitis
Suspect
CNS infection (meningitis, encephalitis, abscess) in patients with
altered LOC, until these conditions are either ruled out or another
cause is identified. Fever, nuchal rigidity, and/or focal neurological
changes are highly suggestive of CNS infection.
PEDS: Very young children may exhibit subtle signs, such as listlessness, poor feeding, and irritability. There may be grunting respirations. Seizures are common. A bulging fontanelle is a late and inconsistent finding. A child with meningeal irritation may wish to lie in a fetal position. When meningococcemia is occurring, you may see a distinctive purpuric rash. Hypoglycemia may be present. Cerebral edema may be present.
The impression of an experienced examiner, while not perfect, is the best single guide to the presence of CNS infection in this age group. In neonates and young infants (age 0 to 3 months), clinical evaluation may be difficult.
Lumbar puncture (LP) is the best diagnostic test for
meningitis. Because of the theoretical risk of herniation in the face
of elevated intracranical pressure (ICP), many practitioners prefer to
perform a CT scan prior to LP. CT scanning has not been
proven absolutely necessary nor 100% effective for this purpose. Most
experts now recommend obtaining blood cultures and starting antibiotic
treatment before either CT or LP in patients where meningitis is
strongly suspected.
Geriatric patients frequently have minimal physical findings, other than a decreased LOC.
See Vol III—IN2 Meningitis for further discussion of CNS infection.
Initial Management
-
Administer oxygen and protect the airway.
-
Establish an IV.
-
Draw a blood culture and routine labs. Begin antibiotic IV therapy as soon as the diagnosis of bacterial meningitis is seriously considered.
-
Septic shock may be present. Initiate volume loading with normal saline, 1 to 2 liters in adults and (PEDS) 10 to 20 mL/kg in children. Take care not to overshoot the mark, which would result in cerebral edema.
-
If seizure activity, papilledema, or any focal neurologic finding is present, obtain a CT scan of the head as soon as possible to rule out mass effect of a brain abscess or severe cerebral edema. If these are not found, (PEDS) perform a L4-L5 lumbar puncture in neonates and a L3-L4 lumbar puncture in older children and adults to obtain spinal fluid for culture and examination for cells and glucose.
Systemic
inflammatory response syndrome (SIRS). Two of the
following
signs of inflammation:
a. Temp > 100.9°F (38.3°C) or < 96.8°F (36°C)
b. Heart rate > 90 bpm
c. Respiratory rate > 20 or PaCO2 32 mm Hg
d. WBC > 12 000, < 4000, or > 10% bands
Sepsis—SIRS
resulting from infection (bacterial, viral, fungal, or
parasitic)
Severe Sepsis—Sepsis
associated with signs of at least one organ
dysfunction, hypoperfusion, or hypotension.
Septic Shock—Sepsis-induced
hypotension persisting despite adequate
fluid resuscitation.
Multi-organ
dysfunction—Presence of altered function of 2 or more
organs in an
acutely ill patient such that hemostasis cannot be maintained without
intervention.
Severe sepsis and septic shock usually manifest as fever, obtundation, hypotension, and weakness. Severe sepsis may also cause altered LOC. An inappropriate dilatation of the vascular space results in relative hypovolemia. This results in poor filling of the heart and an inadequate cardiac output, even though there is a compensatory tachycardia. In the first phase of septic shock (warm), the patient may have warm skin and diaphoresis. In the second phase (cold), the patient is cool and vasoconstricted. The patient may appear ashen because of poor peripheral perfusion. Reduced myocardial contractility may also be present in severe sepsis. Acute myocardial infarction can result if the patient has coronary artery disease. The presentation of sepsis in geriatric patients is particularly subtle. PEDS: The presentation of sepsis in children < 3 months is also particularly subtle. Perform a LP as part of the sepsis work-up in neonates.
Clues for the origin of the severe sepsis are sometimes apparent cutaneously. Toxic shock resulting from staphylococcal infection is accompanied by a faint red rash. Gas gangrene infections are accompanied by a bronzing of the skin over the infected area. Necrotizing fascitis can produce an erythema of the overlying skin. Meningococcemia is accompanied by a purpuric rash. Palpation of the whole body may reveal areas of tenderness over the site of infection. Pulmonary, renal, and abdominal infections are common sources of septicemia. PEDS: Volvulus of the gut and intussusception may also result in septicemia in children, even without abdominal findings.
Initial Management
-
History and physical exam
- Laboratory studies
- Blood cultures (at least 2 with one drawn percutaneously and one drawn through each vascular access device if in place > 48 hours)
- Cultures of urine, CSF, sputum, wound or other body fluids
- CBC, coagulation, BUN, Cr, HCO2, liver enzymes, amylase, UA
- Lactate (if greater than 4 mmol/L = severe sepsis)
Initial Resuscitation
-
Administer oxygen and protect the airway. If the patient is intubated, culture any purulent sputum obtained.
-
Fluids – Give 500 to 1000 cc of crystalloid over 30 minutes then re-evaluate. Septic shock patients may require 6 to 10 liters of fluid in the first 24 hours. If after initial fluid bolus, the patient continues to be hypotensive (septic shock) or shows signs or at least one organ dysfunction or elevated lactate (> 4 mmol/L) (severe sepsis), initiate Early Goal-Directed Therapy. (See guidelines that follow.)
PEDS: In children, give 20 mL/kg of NS. -
Antibiotics—Give broad-spectrum antibiotics within the first hour after diagnosis of sepsis (after cultures obtained)
-
If after initial fluid bolus, the patient continues to be hypotensive (septic shock) or shows signs or at least one organ dysfunction or elevated lactate (> 4 mmole/L) (severe sepsis), initiate early goal-directed therapy (below).
Early Goal-Directed Therapy
-
Place central line for monitoring central venous pressure (CVP) and central venous O2 saturation. Vol II—Circ Skills 2 Central Venous Access)
Fluid Resuscitation. Administer 500 cc boluses of NS until CVP is 8 to 12 (12 to 15 in mechanically ventilated patients). If unable to monitor CVP, continue fluid resuscitation until there is subtle evidence of intravascular volume overload (ie, basilar rales on lung auscultation or a decrease in pulse oximetry). Central venous access is essential in geriatric patients to avoid over-hydration and pulmonary edema. Vol II—Circ Skills 3 Central Venous Pressure Measurement)
Measure central venous O2 saturation (either by continuous monitor or individual sample). If central venous O2 saturation < 70, check Hgb. If < 10, transfuse 1 unit of PRBC. If > 10, start inotropic therapy with dobutamine (2 to 20 μg/kg/min; titrate so heart rate does not increase by > 10% of baseline—preferred, especially if the patient is already receiving norepinephrine as a vasopressor) or dopamine (2 to 20 μg/kg/min titrated to the desired effect). Premature use vasoconstrictors may result in renal failure and severe peripheral ischemia; be sure that the optimal effect of volume loading has been achieved before resorting to this treatment. Also consider intubation and mechanical ventilation.
Vasopressor therapy. If the patient remains hypotensive despite adequate fluid resuscitation, place arterial line. If mean arterial pressure (MAP) is < 65, begin vasopressor therapy with norepinephrine or dopamine. Note: Give vasopressors through a central line, and place an arterial line in all patients receiving vasopressors. Maintain MAP of 65 to 90. If unable to provide arterial line or CVP monitoring, consider early transfer to tertiary level ICU.
Recombinant Activated Protein C (Xigris). Consider giving this to patients who are at high risk of death (Apache score > 25, sepsis-induced multiorgan dysfunction, or sepsis-induced acute respiratory failure and with no contraindication to absolute bleeding risk).
Glycemic control. Maintain blood glucose < 150. This may require a continuous insulin infusion.
DVT prophylaxis. Give severe sepsis patients deep vein thrombosis prophylaxis with either low dose unfractionated heparin (5000 units SQ every 12 hours) or low molecular weight heparin (Lovenox 30 mg SQ every 12 hours)
Stress ulcer prophylaxis. Administer a proton pump inhibitor or H2 blocker to prevent stress ulcers.
Mechanical ventilation in acute lung injury (ALI)/ARDS. In patients who are mechanically ventilated, use low tidal volumes (6 mL/kg of predicted body weight) with the goal of maintaining end-expiratory plateau pressures of < 30 cm H2O. Vol III—IN3 Sepsis in Adults, Vol I—Pathway 6 Adult Respiratory
Pneumonia may present as
a decreased LOC at the extreme ages of life. Even without abnormal
physical findings, it is important that pneumonia be ruled out in all
patients with a decreased LOC.
Urosepsis
Urosepsis may be the
underlying source of the infection causing a decreased LOC. PEDS: Be
highly suspicious of this in young children and in
geriatric patients.
A very resistant bacteria may be the cause of urosepsis in
institutionalized geriatric patients.
P—POISONING, PSYCHOGENIC POISONING (DRUG OVERDOSE, TOXIC
EFFECTS)
Please Note: Many types of poisoning may cause altered LOC. Only the more common causes as a primary effect are discussed here. Always be aware of co-ingestants. For more information, see Vol III—Toxicity Portals (particularly TOX1 Systematic Approach).
Acetaminophen Overdose
Acetaminophen
overdose can result in fatal hepatotoxicity. In adults and adolescents,
hepatotoxicity may occur following ingestion of 7.5 gram (24 regular
strength or 15 extra-strength pills). PEDS: Younger children are
less
subject to this complication, but it does occur. The
patient is usually
free of severe symptoms but may exhibit flu-like symptoms.
Initial Management
-
If the ingestion has occurred within the previous 90 minutes, administer activated charcoal (AC).
-
Consider this diagnosis in all cases of overdose. The potentially fatal hepatotoxicity can be prevented by administering N-acetylcysteine before symptoms appear. See Vol III—TOX3 Acetominophen Overdose.
Aspirin Overdose (Vol III—TOX4 Aspirin Overdose)
Aspirin overdose is often exhibited in a physiologic state requiring emergency critical care. In such cases, 300 mg/kg or more has been ingested. Nausea, vomiting, epigastric pain, hyperthermia, confusion, coma, and seizures may occur. Hypokalemia, anion-gap acidosis (Vol III—END/M6 Acid-Base), and high or low glucose levels may be present. The patient may complain of tinnitus. Tachypnea may be present. Attempt to determine whether the patient is chronically overdosing with aspirin. If this is the case, serum salycilate levels correlate poorly with the degree of toxicity present. Patients who are chronically ill are prone to develop pulmonary edema.
Initial Management
-
Administer oxygen and protect the airway as necessary.
-
Start IVs.
-
Treat seizure activity. (Vol III—NEU1 Status Epilepticus)
-
Insert a large bore orogastric tube (30 to 40 French) and lavage the stomach with tap water (only if the ingestion has occurred 1 hour prior to administration).
-
After lavage, administer AC.
-
Begin a volume load of 1 to 2 liters normal saline in adults and (PEDS) 10 to 20 mL/kg in children.
-
Administer 0.5 to 1.0 mEq/kg sodium bicarbonate IV. Monitor blood gases to maintain a pH of 7.4 to 7.5.
-
Monitor the ECG for signs of hypokalemia: low voltage, flattened T waves, increased QT interval, U waves. Add 20 mEq potassium to each liter of fluid if the potassium levels are low.
-
Place a Foley catheter.
-
Once rehydrated, use D5 ½ NS and add 100 mEq sodium bicarbonate to each liter bag. Administer at a rate to achieve a urine output of about 1 to 1.5 mL/kg/h.
-
Pulmonary edema due to capillary leak needs to be monitored carefully.
Tricyclic Overdose (Vol III—TOX 5 Tricyclic
Antidepressants)
Tricyclic
antidepressants may cause sudden deterioration in LOC, cardiovascular
collapse, and seizures. Patients are notorious for their propensity to
suddenly crash after appearing well. Any ingestion over 10 mg/kg or of
unknown quantity constitutes grounds for concern and immediate action.
Widening of the QRS > 0.1 second, sinus tachycardia, torsades de
pointes, and anticholinergic effects such as dry mouth, dilated pupils,
and hot red skin also point to tricyclic intoxication. Anticholinergic
symptoms are described as: Red
as a beet, Dry
as a bone, Hot
as a hare,
and Mad as
a hatter. The patient may seize or suffer a dysrhythmia at
any time, so prepare for the worst.
Initial Management
-
Administer oxygen and protect the airway. RSI may be of great use. (Vol III—AIR1 Rapid Sequence Intubation)
-
Perform gastric lavage, followed by at least 50 g of AC.
-
Start IVs.
-
Apply ECG leads and an O2 sat monitor. Check the length of the QRS interval. If it is prolonged (> 0.1 sec or 2.5 little squares), administer sodium bicarbonate 1 mEq/kg IV as a bolus/load, followed by a drip to titrate the pH into an alkalotic range of 7.45 to 7.5. PEDS: Use the same dose for pediatric patients. If the QRS interval is > 0.16 sec or 4 little squares, seizures and dysrhythmias are likely.
-
If the QRS interval is not prolonged and the patient is cooperative, administer AC, then insert a large bore (36 to 42 French) orogastric tube and lavage out the AC while watching the monitor for evidence of QRS widening. After lavage, administer AC again.
-
If the patient seizes, intubate the trachea (if not already done). Terminate the seizure with diazepam. (Vol III—NEU1 Status Epilepticus)
-
Dysrhythmias are common. Sodium bicarbonate is the most effective treatment.
-
Treat hypotension with the Trendelenburg position and IV fluids. Measure CVP (Vol II—Circ Skills 3 Central Venous Pressure Measurement) and aim for a pressure of 10 to 15 cm H2O. The use of vasopressors (eg, norepinephrine 4 mg/500 cc D5W at 0.1 to 0.2 μg/kg/min) may be necessary for hypotension unresponsive to fluids. Do not use dopamine because its beta effects may exacerbate the beta-mediated effects of the tricyclic agent on the heart and vasculature. Intra-aortic balloon pumping may be indicated.
Anticholinergic Drug Overdose
Anticholinergic
drugs such as atropine, scopolamine, and the antihistamines may cause
changes in mental status, along with hot red skin, tachycardia, dry
mucosa, and dilated pupils. Treatment is usually supportive. But, in
cases of seizure or coma, consider physostigmine. The dose is 1 mg IV
over at least 2 minutes. PEDS:
Children 0.02
mg/kg over at least 2 min
(neonate dose is unknown).
This may be repeated every 10 to 20 minutes
until therapeutic effect manifested as the anticholinergic toxic
effects resolve. Do not use physostigmine for tricyclic antidepressant
overdose.
Benzodiazepine Overdose
Benzodiazepine overdose
commonly causes altered LOC. Monitor respiratory depression and
administer AC. Consider using the antidote flumazenil only after
complete patient evaluation and consideration of flumazenil’s risks.
(Vol
III—TOX8 Benzodiazepine Overdose)
Hypnotic Drug Overdose
Hypnotics/sedatives
are a broad group of drugs (barbiturates and non-barbiturates) that are
commonly abused and/or used for suicide attempts. Co-ingestants are
common. ABC management and limiting further absorption are necessary
but insufficient interventions. Use drug levels in critical patients to
guide selective aggressive therapy for specific interventions, such as
alkaline diuresis for symptomatic barbiturate overdoses or hemodialysis
for chloral hydrate overdose. Sodium bicarbonate (1 to 2 mg/kg IV over
2 minutes) followed by 100 mg/L D5 ½ NS at a
rate of 2 to 3 cc/kg/h may
be used to alkalinize the urine to facilitate barbiturate excretion.
Methamphetamine Intoxication (Vol III—TOX13 Amphetamine
Analog
Intoxication)
Methamphetamines
are the most commonly used designer drugs today and are easily
synthesized by adding a chemical substrate to the phenyl ring of
amphetamine or methamphetamine. Clinical effects include
hallucinations, paranoia, heightened energy level, and severe
agitation. Life-threatening adverse effects include arrhythmias,
hyperthermia, hypertensive crisis, myocardial infarction,
cardiovascular collapse, seizures, and respiratory failure.
Initial Management
-
Use benzodiazepines for control of seizures and agitation, keeping in mind that a very large dose of benzodiazepines may be necessary to control the patient’s symptoms.
-
Use a vasodilator (eg, nitroprusside) or an alpha/beta antagonist (eg, labetalol) or an alpha antagonist (eg, phentolamine) for the treatment of hypertensive crisis.
-
Use active cooling measures to treat drug-induced hyperthermia.
-
Administer intubation and paralysis to manage respiratory failure and to help reduce muscle rigidity that contributes to severe hyperthermia.
-
Carefully monitor for and treat severe electrolyte imbalance, metabolic acidosis, and disseminated intravascular coagulation.
-
Consult early with a clinical toxicologist to help with the management of difficult patients.
Carbon Monoxide Poisoning
Consider
carbon monoxide poisoning in patients exposed to smoke, fumes, or fire
as well as in patients for whom headache is prominent and where
companions and/or family members are similarly affected. Diagnosis is
by blood levels; start treatment with 100% O2 by
non-rebreather or ET
tube pending the return of the CO level. Use hyperbaric treatment for
serious situations or high CO levels. (Consult the nearest hyperbaric
team.) (Vol
III—TOX15 Carbon Monoxide Poisoning)
Cyanide Poisoning (Vol
III—TOX17 Cyanide Poisoning)
Cyanide
poisoning should be suspected in the following instances: suicide
attempts, industrial accidents, or exposure to products of combustion.
Suspect cyanide poisoning in smoke inhalation or burn victims whose CO
levels do not accurately reflect their clinical picture. Most serious
cases of cyanide toxicity are manifested by seizures, coma, shock, and
cardiac arrest. Do not wait for lab results before treating cases that
you suspect are life-threatening. The most common treatment has 3
components (usually found in a cyanide antidote kit): amyl nitrate
inhalation from “popper” ampules; 3% sodium nitrite slow IV push (adult
and PEDS: 0.33 cc/kg up to 10 cc);
and sodium thiosulfate 12.5 g IV at
3 to 5 mL/min (PEDS:
412.5 mg/kg IV
at 3 to 5 mL/min).
A newer, more expensive treatment, called the Cyanokit™ (containing the drug hydroxocobalamin) is now available in the United States. In the presence of cyanide, Cyanokit’s active drug takes up the cyanide and becomes a form of vitamin B12. The starting dose of hydroxocobalamin for adults is 5 g (ie, both 2.5 g vials) administered as an IV infusion over 15 minutes (approximately 15 mL/min or 7.5 min per vial).
Organophosphate (Insecticide)
Organophosphates
occur in pesticides and nerve gas. Organophosphates inhibit the enzyme
acetylcholinesterase resulting in the accumulation of acetylcholine at
muscarinic and nicotinic receptors.
Presenting symptoms may occur from within just a few minutes to 12 hours post exposure. Organophosphates are lipid soluble so patients will develop muscarinic symptoms first and then progress to nicotinic and CNS symptoms. Hypersecretion occurs due to hyperactivity of the gut and the bronchial muscles. Patients secrete copious amounts of fluids from every orifice. Effects on the brain may produce staggering gait, severe tremor, and a psychosis that may be mistaken for alcohol intoxication. See Vol III—TOX18 Organophosphates Toxicity.
Quick recognition of symptoms is necessary to reverse cholinergic effects. Sudden unconsciousness may be attributable to heat exhaustion, but may potentially be a result of organophosphate exposure. Miosis and muscle twitching are symptoms not seen with heat exhaustion but seen with organophosphate exposure.
Initial Treatment
-
Emergency workers are at risk of becoming poisoned themselves when caring for an organophosphate poisoned patient. Team members should wear rubber gloves and protective gowns to avoid contamination.
-
The first job is to decontaminate the patient. All types of clothing absorb organophosphates, so remove and decontaminate all clothing to prevent further exposure. Place clothing in a container that can be sealed. Wash the patient with soap and water 3 times. If there has been ocular exposure, irrigate the eyes with a copious amount of tap water for 15 minutes.
-
Syrup of ipecac is contraindicated. Perform gastric lavage followed by activated charcoal. Because some organophosphates are carried in hydrocarbon-based solvents, use a cuffed ET tube to prevent aspiration.
-
Administer oxygen and intubate the patient if there is a decreased level of consciousness or if tracheal and pharyngeal secretions threaten the airway.
-
Obtain IV access.
-
Obtain an ECG.
-
Medications. Atropine blocks the action of acetylcholine. 2-PAM treats the muscle weakness and blocks the action of acetylcholine but atropine is cheaper and more readily available to start treatment. Atropine may be given up to 1 to 2 grams in severe cases. Give until mucus membranes are dry.
-
Atropinization. Consider for all patients with significant cholinergic symptoms. Adult Dose: 1 to 2 mg slow IV push and PEDS Dose: 0.015 to 0.05 mg/kg slow IV push. Doses may be repeated every 15 minutes as needed, and doses can be doubled (2 to 4 mg). Atropine drips may also be used at 0.5 to 2.4 mg/kg/hour.
-
The endpoint of therapy is drying of secretions (nasal, oral). Atropine may also be given via subcutaneous, ET, and intraosseous routes. For severe poisonings, therapy may be required for 48 hours. Note: Atropine does not reverse muscle weakness or respiratory failure.
-
Pralidoxime (2-PAM). 2-PAM reverses the phosphorylation of the cholinesterase molecule. It should be given within 24 hours but may be effective up to 36 to 48 hours. If use of atropine indicates an OP exposure, administer 2-PAM concurrently. Adult Dose: 1 gram IV and PEDS Dose: 25 to 50 mg/kg in 200 mL D5W or NS over 15 minutes. Too rapid exposure can result in tachycardia, muscle rigidity, and neuromuscular blockade. The dose may be repeated in 1 hour and every 6 to 12 hours for 24 to 48 hours if symptoms are still present.
-
The endpoint of therapy is resolution of coma and fasciculations. Note: Highly fat-soluble compounds may require longer therapy. Continuous infusion of 500 mg/hour or 10 to 25 mg/kg every 8 hours may be used.
-
Terminate seizures with diazepam.
-
Pralidoxime (2-PAM) is the specific antidote for muscle weakness/paralysis, but atropine is cheaper and more readily available to start treatment. Initial dose 1 to 2 g slow IV push (in severe cases) over 15 min. Give until mucous membranes are dry. PEDS: Initial dose 25 mg/kg IV over 30 min. The endpoint of therapy is drying secretions. (Vol III—TOX18 Organophosphates Toxicity)
Iron Ingestions
Iron
ingestions are notoriously difficult to assess. Shock and hepatic
failure can appear after apparent recovery. The pathophysiology of iron
toxicity follows four stages:
Stage 1 GI stage
with vomiting, diarrhea, and abdominal pain.
Stage 2
Relative stability stage that lasts only a few hours. The
patient may be acidotic and poorly perfused.
Stage
3 Shock stage with circulatory failure, profound
hypotension, lactic
acidosis, and hypovolemia. This stage may result in death.
Stage 4
Hepatotoxicity stage appears within 48 hours and may be fatal.
Iron levels < 300 μg/dL drawn 2 to 6 hours after the ingestion predicts a benign course. Levels > 500 μg/dL predict a severe course.
Initial Management
-
When the patient has severe symptoms, aggressive supportive management is needed for all of the manifestations of toxicity. Address hypovolemia and shock aggressively, obtaining frequent blood gases to guide treatment for acidosis. Large amounts of sodium bicarbonate may be needed to treat acidosis.
-
Whole bowel irrigation may be indicated.
-
After blood volume has been restored to normal, begin chelation therapy with deferoxamine. (Vol III—TOX14 Iron Ingestion)
Hydrocarbon Ingestions
Hydrocarbon ingestion may occur at any age, but it is (PEDS) most
common in children and adolescents.
PEDS: Hydrocarbon ingestions by children vary in seriousness according to the hydrocarbon ingested. Gasoline, kerosene, lighter fluid, and many other hydrocarbons are not likely to cause serious problems, but as little as 1 mL of mineral seal oil can be fatal. The most dangerous effect is the ability of these low surface tension chemicals to spread over the moist surfaces of the airway and into the bronchial tree. This results in severe chemical pneumonitis. Suspect intoxication from the presence of characteristic odors, or in the case of paint sniffing, facial colors.
Initial Management
-
Do not administer SOI and AC. Also avoid antibiotic and steroid therapy. The only treatment option is to support ventilation. Observe for at least 6 hours for any developing pulmonary problems.
Psychogenic Coma (Catonic State)
Psychogenic
coma is a diagnosis of exclusion, which is (PEDS) virtually unheard of
in small children. Patients may appear comatose with a
remarkable
ability to deny pain. Common clues include fluttering eyelashes in an
attempt to keep eyes closed (despite interest in the environment) and
feigned seizure activity characterized by thrashing movements rather
than tonic-clonic contractions. If you
have any doubts, a normal EEG confirms the diagnosis. Psychogenic coma
may be an involuntary manifestation of psychiatric illness or willful
malingering.
Initial Management
-
Determine that the patient is physiologically intact with normal vital signs and pupil responses.
-
The well-known ploy of dropping the patient’s arm while it is positioned over his or her face (thus causing the patient to move it aside) is fairly reliable as an indication that the patient is feigning coma.
-
Over time, the patient is unable to resist “regaining consciousness”; simply waiting usually resolves the problem.
S—STROKES, SHUNTS, SHOCK (CNS INSULTS)
Thrombotic or Embolic Strokes (Vol III—NEU2 Stroke)
Thrombotic
or embolic strokes present as an acute neurological deficit, usually
without severe headache or vomiting. Strokes may cause coma depending
on the size and location of the central nervous system damage and the
presence and degree of increased intracranial pressure (ICP).
Initial Management
-
Maintain and protect the airway and administer oxygen
-
Identify and treat increased ICP. Cerebral edema is treated with 20% mannitol, 250 to 500 cc IV rapid bolus.
-
Treat hypertension only if it is sustained at levels > 180/105.
-
Consider early CT brain scanning if the patient is a potential candidate for TPA or heparin therapy. The therapeutic window for treatment is 3 hours from symptom onset, during which exam, stabilization, CT scanning interpretation, and therapy contraindications must be assessed. After 3 hours, the risks from thrombolytics increase and the benefits decrease. Hospitals should have protocols in place in order to utilize this type of therapy.
-
Determine source of embolism if embolic. Consider heparin therapy in select patients.
Intracerebral hemorrhage tends to produce hemispheric signs. The onset of these neurological changes is sudden and frequently accompanied by severe headache, vomiting, and changes in LOC often leading to coma.
Initial Management
-
Protect the airway (with the patient ventilated if necessary).
-
Severe hypertension may need treatment, but hypotension must be avoided. Lower severe hypertension to about 180/105; do not try to normalize. (Vol III—CV13 Hypertensive Crises)
-
If there are signs of increased ICP with lethargy, obtain a head CT scan. If increased ICP is present, hyperventilate and administer mannitol 1 g/kg IV or hypertonic saline. (Vol III—NEU5 Increased Intracranial Pressure)
-
Consider cerebellar involvement if the patient presented with or noted dizziness and truncal ataxia on ambulation at the start of symptoms. This may indicate hemorrhage into the cerebellum. This is a true emergency because unless decompressed, this mass may result in sudden death. Obtain a head CT scan and neurosurgical consult.
Subarachnoid Hemorrhage (Vol III—NEU5 Increased Intracranial Pressure)
Subarachnoid
hemorrhage is more common in women overall, but under the age of 40,
subarachnoid hemorrhage is more common in men. The onset is gradual or
immediate with severe headache and vomiting. Frequently, there is
nuchal rigidity. In cases of massive subarachnoid hemorrhage with
decreased LOC, diagnose by CT scan. In as many as 10% of patients with
smaller bleeds, CT scans may be negative, and a LP or cerebral
angiogram is required for diagnosis. The most common etiology is due to
a ruptured or leaking berry aneurysm. About 6% of the time, the
etiology is a leaking arteriovenous malformation.
Initial Management
-
Frequently there is severe hypertension. If the patient has a systolic blood pressure > 220 torr or a diastolic pressure > 120 torr, carefully lower pressure with labetolol 20 mg IV every 10 to 20 minutes. For patients with diastolic pressure >140 torr, use a nitroprusside drip starting at a rate of 0.5 μg/kg/min.
-
Seizures must be prevented. Administer a phenytoin load 15 to 20 mg/kg at a rate no faster than 50 mg/min or administer fosphenytoin 18 mg PE/kg IV over 10 minutes. (Vol III—NEU1 Status Epilepticus)
-
Treat nausea and vomiting with an antiemetic such as ondonsetron 4 mg slow IV push or prochlorperazine 5 mg slow IV push.
-
Nimodipine (a Ca ++ channel blocker) 60 mg PO/NG every 6 h may reduce vasospasm and improve outcomes. Give nimodipine ONLY by mouth or through an NG tube. NEVER give nimodipine via IV administration, which can result in death, near-death, cardiac arrest, and severe declines in blood pressure. If a patient is unable to swallow the capsule, give via NG tube by making a hole in both ends of the capsule with a standard 18-gauge needle. Remove the contents of the capsule, and empty the contents into the syringe. Note that a standard needle does not fit an oral syringe and must be attached to an IV syringe. Clearly label the IV syringe “Not for IV Use,” and then remove the needle. Then, empty the syringe contents into the NG tube followed by 30 mL of NS.1
-
Consult with a neurosurgeon.
Subdural Hematoma
Subdural
hematoma is usually caused by venous interruption beneath
the dura with
the blood spreading out under the dura. Typical history is that of
trauma with temporary loss of consciousness with residual headache,
personality change, or abnormal neurologic findings. The subdural
hematoma may be (1) acute with deteriorating LOC and neurologic status
within 24 hours of the injury, (2) sub-acute with symptoms apparent in
2 to 14 days of the injury, or (3) chronic form with symptoms
recognized > 14 days after the injury. PEDS: Consider a
diagnosis of
subdural hematoma in infants and children when abuse is a possibility.
Initial Management
-
The airway must be carefully managed.
-
If increased ICP is present, determine the cause and treat the ICP.
-
Consult with a neurosurgeon.
Epidural Hematoma (Vol II—Disab Skills 1
Skull Trephination)
Epidural
hematoma is classically suspected in a patient who sustains head
trauma, has a short period of unconsciousness, and then appears normal.
After a period of minutes to hours, the patient develops signs and
symptoms of increased ICP due to the arterial bleeding causing an
extra-dural hematoma, which bulges inward. The patient develops
decreased level of consciousness, pupillary changes, and often a
hemiplegia.
Initial Management
-
Protect the airway and ventilate if needed.
-
Rapid evacuation of the epidural hematoma with a trephine may be lifesaving.
Increased Intracranial Pressure
Increased
ICP from any origin causes a decrease in cerebral profusion pressure
(the difference between ICP and the mean blood pressure), resulting in
a decrease in cerebral blood flow leading to cerebral anoxia. Initially
the patient becomes drowsy but with progressive increase in the ICP. If
left untreated, herniation syndromes (uncal or transtemporal) lead to
irreversible brain stem damage. Suspect increased ICP in comatose
patients with hypertension, widened pulse pressure, and abnormal
respiration pattern. Third nerve findings with pupillar dilatation and
sluggish reactivity progresses to hemiparesis, decorticate posturing,
decerebrate posturing, and finally, apnea, hypotension and cardiac
arrest.
Initial Management
-
Secure the airway (Vol II—Air Skills 4 Rapid Sequence Intubation); continue sedation.
-
Consult with a neurosurgeon about whether to use mannitol or hypertonic saline in a patient with increased intracranial pressure.
(Vol III—NEU4 Phenytoin and Fosphenytoin Loading) -
Give prophylactic anti-seizure medication.
-
Treat the underlying cause for the increased ICP.
-
If uncal herniation is occurring despite these measures, consider/ perform emergency trephination on the side of the dilated pupil. (Vol II—Disab Skills 1 Skull Trephination)
-
Obtain CT scan (if feasible/stabilized), and consult neurosurgery. (Vol III—NEU5 Increased Intracranial Pressure)
Shock
Shock of any origin results in a decrease in cerebral blood flow,
cerebral anoxia, and decreased LOC.
Initial Management
-
Maintain the airway and ventilate with oxygen if needed.
-
Identify and treat the cause for shock. (Vol I—Acute Care Portals Shock Acronym—SHRIMPCAN; Vol III—Trau Care 2 Shock)
Shunt Malfunction
If
a ventriculoatrial or ventriculoperitoneal shunt is present under the
scalp in the setting of coma or decreased LOC, immediately determine
the patency of the shunt. To check for shunt patency in shunts with one
palpable chamber, occlude the
tubing proximal to the chamber with one finger and press on the
chamber. If the chamber empties, the shunt is open distally. Now
release finger pressure on the occluded tubing, and the chamber should
fill again. If it does not, there is proximal obstruction. Family
members can usually describe the procedure used to clear an obstruction.
If two chambers are palpable, occlude the proximal chamber with finger pressure while pressing on the distal chamber. If the distal chamber does not empty, there is distal obstruction of the shunt. Now release finger pressure on the proximal chamber while maintaining pressure on the distal one. If the proximal chamber does not fill, there is a proximal obstruction.
In cases of impending herniation or suspected infection, shunt chambers may be aspirated (and cultured). PEDS: In children, the ventricle itself may be aspirated. Consult a neurosurgeon before undertaking these procedures.
If the patient is stable, obtain a CT scan, looking for evidence of acute hydrocephalus/increased ICP.
If a herniation syndrome is in progress with deepening coma and posturing, move ahead and puncture into the dilated ventricle using a 20-gauge needle through or alongside the tubing through the brain. PEDS: In a child with a shunt entering through the anterior fontanelle, direct the needle toward the inner canthus of the ipsilateral eye from the edge of the fontanelle. Stop when cerebrospinal fluid (CSF) returns. Leave the needle in place for continued decompression until seen by a neurosurgeon. Ascending infection is a concern for patients with shunts. Obtain neurosurgical consultation whenever patients exhibit signs and symptoms suggestive of meningitis.
A—ALCOHOL (INTOXICATION, WITHDRAWAL, TOXIC EFFECTS)
Ethyl Alcohol Intoxication
Ethyl
alcohol (ETOH) intoxication may be life threatening because of
respiratory depression and airway compromise, particularly with
vomiting. While alcohol intoxication is a common cause of decreased
LOC, the presence of ETOH does not rule out other coinciding
conditions. Chronic alcoholic patients may demonstrate a variety of
disorders besides intoxication that decrease their LOC. PEDS: In
children and adolescents, ETOH may cause hypoglycemia.
These patients
need careful observation and serial exams throughout their course of
stay.
Blood
alcohol levels are helpful but are not well correlated with the degree
of decreased LOC. Chronic alcoholics may appear relatively normal with
high blood alcohol levels, (PEDS)
while children
and adolescents may be
deeply comatose with lower levels. Treatment is generally
supportive in
pure ETOH intoxication, with special attention to protect the airway
and ensure ventilation. Rule out head trauma. A head CT may be
indicated.
Ethyl Alcohol Withdrawal
A patient in ethyl alcohol
(ETOH) withdrawal presents with delirium, tremors, elevated heart rate
and/or BP, and sometimes elevated temperature or seizures. Severe ETOH
withdrawal can be a life-threatening condition. Benzodiazepines are the
chemical mainstay of withdrawal management: Give diazepam 5 to 10 mg IV
bolus every 5 to 15 min until sedated. PEDS: 0.05 to 0.3 mg/kg/dose
IV
(not to exceed 5 mg/dose) over 2 to 3 min every 15 to 30 min until
sedated. Aggressive supportive measures and adjunctive
treatment with
magnesium and thiamine replacement are often required. (Vol
III—TOX9
Alcohol Withdrawal)
Methanol Intoxication (Vol
III—TOX10 Toxic Alcohols)
Methanol
is commonly found in windshield washer fluid. Methanol intoxication
mimics ethanol intoxication, but abdominal pain and visual disturbances
are frequent. Blindness and coma can result. The laboratory test for
blood alcohol is specific for ethanol so consider methanol intoxication
if the patient seems more inebriated than the blood alcohol level
suggests. An anion gap acidosis is a prominent diagnostic clue.
Initial Management
-
Begin treatment without laboratory confirmation in methanol ingestion.
-
Administer thiamine 50 to 100 mg IV every 6 hours. PEDS: 0.25 to 0.50 mg/kg IV in first 24 h
-
For methanol ingestion administer folate 50 mg IV every 4 hours.
-
Administer 125 mL of 50-proof (50%) ethyl by nasogastric tube to provide ethanol to compete with the methanol for alcohol dehydrogenase in the liver. This enzyme converts methanol into the toxic metabolites, formaldehyde, and formic acid. Continue running fusion of 20 mL/h.
-
Hemodialysis and ethanol IV may be needed. If administered IV, use 10% ETOH in D5W: 10 cc/kg over 30 to 60 minutes as IV loading dose, then 1 to 2 cc/kg/h to maintain blood level of 100 to 150 mg/dL.
-
If Antizol is available, the dose is 15 mg/kg IV over 30 minutes then 10 mg/kg IV every 12 h X 4 doses, then 15 mg/kg IV every 12 h.
PEDS: Suggested doses are the same. -
Also give pyridoxine 50 to 100 mg IV every 6 h. PEDS: 1 to 2 mg/kg IV in first 24 h.
-
Contact a toxicology consultant or poison control center early.
Ethylene Glycol Intoxication
Ethylene
glycol intoxication is similar to methanol intoxication in presentation
and management. PEDS: Unfortunately,
ethylene glycol is found in
antifreeze solution, a sweet-tasting substance that may attract
children as well as adults looking for an ethanol substitute. Like
methanol, the metabolites are formaldehyde and formic acid. Ethanol
competes for the enzyme system that produces these toxic metabolites.
An anion gap acidosis is prominent. Antifreeze solutions usually contain fluorescein that can be detected in the urine with ultraviolet light.
Initial Management
-
Treat the patient in exactly the same way as for methanol ingestion.
-
Hemodialysis and IV ethanol may be needed.
Isopropanol Intoxication
Isopropyl
alcohol (rubbing alcohol) is an intoxicant more potent but similar in
effect to ethanol. In large doses or (PEDS) young children,
isopropyl
alcohol may cause coma, acidosis, and hypoglycemia. Isopropanol
produces hemorrhagic gastritis with abdominal pain and sometimes
bleeding. Treatment is supportive, with emergent hemodialysis for blood
levels > 400 mg/dL or hypotension refractory to fluids and
pressors.
E—EPILEPSY, ENCEPHALOPATHY (HYPERTENSIVE CRISIS, HEPATIC)
Status Epilepticus (Vol III—NEU1
STATUS EPILEPTICUS)
Status
epilepticus is defined as a seizure lasting 30 minutes or 2 seizures
occurring sequentially without an intervening period of normalcy. To
fit the criteria, the seizures may be grand mal, partial, or even
non-convulsive.
Initial Management
-
Apply oxygen. Suction the mouth if needed and insert an oral airway if possible.
-
If the patient is not breathing adequately, ventilate with a BVM. Airway management by intubation, usually with RSI, may be needed either for status itself or for apnea in the post-ictal period. Remember that a patient paralyzed from neuromuscular blockers may still have deleterious electrical seizure discharges occurring in the brain, and needs immediate anticonvulsant therapy.
-
Establish an IV. In adults, administer thiamine 100 mg IV if appropriate. Follow this with 50 mL of 50% glucose, unless a bedside test for blood glucose reveals no hypoglycemia.
-
To stop a seizure, the initial treatment of choice is a benzodiazepine such as lorazepam: 4 mg IV or IO over 2 to 5 min; repeat in 10 to 15 min prn. PEDS: 0.1 mg/kg (up to 4 mg) IV over 2 to 5 min; repeat with ½ dose in 10 to 15 min prn. If ineffective, phenobarbital, valproic acid, phenytoin/fosphenytoin, or other agents may be used. (See Acute Care Portals, Status Epilepticus Treatment Plan.)
-
If the seizure continues, consider such etiologies as hypoglycemia, hyponatremia, hypernatremia, hypocalcemia, hypomagnesemia, pyridoxine deficiency, and isoniazide toxicity.
-
Terminate the seizures of hypoglycemia in adults with 50% dextrose 0.5 to 1.0 g/kg IV. PEDS: In infants and small children, give 2 to 4 mL/ kg of D25 IV. Neonatal: 2 to 4 mL /kg of D10. Premature Neonates: 1 to 2 mL /kg of D10.
-
Terminate the seizures of hyponatremia with 6 mL/kg of 3% NaCl.
-
Terminate the seizures of hypocalcemia with a 5 to 10 mL slow push of a 10% solution of calcium chloride and (PEDS) 0.2 mL/kg up to 10 mL in children.
-
Terminate the seizures of hypomagnesemia with 4 grams of magnesium sulfate IV in adults and (PEDS) 50 mg/kg in children up to 4 grams over 10 minutes.
-
If the patient is taking isoniazide (INH) or has access to isoniazide, administer 1 gram of pyridoxine (vitamin B6) IV for each gram of INH ingested. Otherwise, give 50 to 100 mg pyridoxine IV in case the patient is deficient.
-
Paralysis and anesthesia may be required for very resistant cases.
-
A seizure is often a foreboding symptom of some other illness, such as meningitis or drug or substance overdose. Once the seizure is stopped, repeat this pathway to bring all possible causes to mind.
Hypertensive Encephalopathy (Vol
III—CV13 Hypertensive Crises)
Hypertensive
encephalopathy (hypertensive crisis) is caused by cerebral
hyperperfusion with loss of normal autoregulation of arterial blood
flow. The blood-brain barrier is compromised, resulting in fluid
movement into the brain. Patients
exhibit lethargy, confusion, and even coma. These patients usually have
a history of recently untreated hypertension with an onset of headache,
nausea, vomiting, visual changes, and obtundation. BP is usually in the
250/150 range, although the absolute value of the BP does not determine
the emergency approach but rather the elevated BP and the patient’s CNS
symptoms. Besides altered LOC, there may be retinal changes, neuro
findings (focal signs, reflex changes, nystagmus), or seizures.
However, it is the evidence of end-organ injury that makes the
diagnosis and not the blood pressure measurement per se.
Initial Management
-
Administer oxygen and protect the airway if necessary.
-
Start an IV and obtain an ECG.
-
Begin a nitroprusside drip 50 mg in 250 mL D5W at a rate of 0.5 μg/kg/min. Increase this rate gradually to achieve the desired blood pressure. Aim to reduce the mean arterial pressure (MAP) by 20% to 25% in 30 to 60 minutes.
MAP = diastolic BP + 1/3 (systolic BP - diastolic BP)
Lowering the blood pressure too much and too fast results in cerebral ischemia.
-
Insert a urinary bladder catheter. Monitor urine output. Some hypertensive patients are volume depleted and need fluids to protect the kidneys from pre-renal failure.
Hepatic Encephalopathy
Hepatic
encephalopathy is seen as a precipitating event in patients with severe
(usually chronic) liver disease. The liver is unable to detoxify CNS
toxins. Signs and symptoms of liver disease are usually present, such
as asterixis, ascites, and jaundice. The precipitating events are
varied: GI bleed, sepsis, CNS depressants, azotemia, hypoxia, and
others. LOC ranges from confusion to coma. Besides the considerable
support necessary in these complex patients for coexisting problems,
specific initial treatment consists of correcting /eliminating the
precipitating factors and giving lactulose: initial dosing 30 to 50 mL
PO every hour until diarrhea OR if unable to give PO, give 300 mL in a
700 mL water retention enema. Consider giving Neomycin 1 g PO.
I—INSULIN AND OTHER HORMONES
Diabetic Ketoacidosis (Vol III—END/M2 Diabetic Ketoacidosis)
Diabetic
ketoacidosis (DKA) is usually exhibited by nausea, vomiting, abdominal
pain, dehydration, hypotension, tachycardia, hyperventilation (or
Kussmaul’s respirations), and a decreased LOC. The breath may smell of
acetone. The blood glucose level is > 300 mg/dL, and the serum
bicarbonate level is < 15 mEq/L with an anion gap. The patient
is
usually a known diabetic, (PEDS:) although this is not necessarily true in children.
Initial Management
-
Administer oxygen and, if the airway is not protected, intubate the patient.
-
Begin a fluid infusion of NS, starting with 1 liter in the first 30 minutes. PEDS: In children, start with 20 mL/kg. Switch to Lactated Ringer’s if more fluid loading is needed in order to avoid hyperchloremic acidosis. Once hemodynamically stabilized, switch fluids to ½ NS. Once blood sugars reach the 200 to 300 mg/dL range, switch to glucose-containing solutions. Five liters may be required to achieve rehydration in adults, so establish a central line to monitor CVP, especially in geriatric patients. PEDS: Children may require several boluses of NS at 20 mL/kg. The single most important therapy for DKA is volume restoration.
-
Even if the serum potassium level is normal in the beginning, total body potassium is low. Monitor the serum potassium hourly, and watch the ECG monitor for signs of hypokalemia. Add KCL to the saline IV.
-
After rehydration is underway, begin a low-dose insulin drip (add 100 units of regular insulin to 100 mL NS) of 5 to 10 units of regular insulin per hour (PEDS: 0.1 units/kg/h in children) and continue until the acidosis and ketonemia have cleared.
-
Because infection is a common cause for DKA, conduct a thorough search for signs of infection, including a chest x-ray, urinalysis, and a neurological exam. Myocardial infarction can also precipitate DKA.
Non-Ketotic HypersmolarComa (Vol III—END/M5
Hyperosmolar State)
Non-ketotic
hyperosmolar coma occurs when the blood glucose level is high in the
absence of ketoacidosis. It occurs in diabetics and is much less common
than DKA. The blood glucose often is > 800 mg/dL. These high
levels
produce hyperosmolarity, dehydration, stupor, and focal or grand mal
seizures. Total body potassium deficiency is usually severe.
Initial Management
-
Administer oxygen and, if the airway is not protected, intubate the patient.
-
Begin a fluid infusion of NS with 1 liter in the first 30 minutes in adults and (PEDS) 20 mL/kg in children. If shock is present, 5 or more liters may be required to restore an adequate blood volume. PEDS: Repeated boluses of 20 mL/kg NS may be necessary in children.
-
As with DKA, begin potassium replacement early and follow the ECG monitor and serum potassium closely.
-
Begin a low-dose insulin drip as with DKA and continue this until the blood glucose is < 300 mg/dL. Begin adding glucose to the IV when the blood glucose is < 250 mg/dL.
Hypoglycemia
Hypoglycemia
may have many causes, but by far the most common cause is insulin
reaction. Patients may exhibit coma, seizures, stupor, hemiplegia,
sweating, hyperventilation, inappropriate behavior, and hypothermia.
Check blood glucose levels in any patient with an altered mental state.
The blood glucose is usually < 50 mg/dL in these cases.
Initial Management
-
Administer oxygen and protect the airway.
-
Start an IV and administer 50 mL of a 50% glucose solution in adults and older children. PEDS: In children, use a 25% solution at 0.5 to 1.0 g/kg (2 to 4 mL/kg). In infants, use 10% dextrose at 2 to 4 mL/kg IV.
Hypoglycemia has already been addressed under DONT. Search for the underlying cause of hypoglycemia.
Ketotic Hypoglycemia
Ketotic
hypoglycemia (PEDS)
in children
results from an inborn error of
metabolism that affects children in the age range of 18 months to 5
years. The attacks of hypoglycemia are sporadic and tend to occur in
the morning.
Initial
Management
These usually respond to the oral administration of glucose.
Addisonian Crisis (Vol III—END/M1 Adrenal Crisis)
Addisonian
crisis (adrenal deficiency) occurs when infection or trauma stresses a
patient with adrenal insufficiency. Commonly these patients are on
chronic steroid therapy with a resulting suppression of the adrenal
cortex. Other causes of adrenal insufficiency are pituitary
malfunction, hemorrhage, and infection (such
as tuberculosis, AIDS). The patient may be confused, weak, and
hypotensive. Nausea, vomiting, and abdominal pain are common. Delirium,
seizures, hyponatremia, hyperkalemia, and hypoglycemia may also occur.
Initial Management
-
When a patient’s history suggests this diagnosis, administer 100 mg of hydrocortisone IV (PEDS: 2 mg/kg in children). Consider this diagnosis in any patient with unexplained hypotension. Repeat this dose every 8 hours under stressful circumstances.
-
Give a 1 to 2 liter NS bolus to adults and (PEDS) 10 to 20 mL/kg to children.
Thyroid Storm (Vol III—END/M4 Thyroid Storm)
Thyroid
storm is a rare, life-threatening event in untreated or
partially
treated thryotoxic patients with a precipitating event or physiologic
stress. Altered LOC ranges from mania to coma. Other clinical aspects
include hypertension, tachycardia, fever, nausea, vomiting, diarrhea,
dehydration, tremor, and thyroid enlargement. No laboratory tests are
immediately available to help in the diagnosis. The physician has to
base treatment solely on clinical grounds.
Initial Management
-
Administer oxygen and protect the airway.
-
Rehydrate with glucose-containing fluids.
-
Initial management is cooling. (See hyperthermia; do not use salicylates.)
-
Give sedation, electrolyte replacement, and hydrocortisone 100 mg IV
-
Begin an IV infusion of the beta blocker propanolol at 0.5 to 1.0 mg/min for 2 to 10 minutes. The cardiac effects should be apparent in 10 minutes with slowing of the heart rate. After 10 minutes, increase rate of infusion by 1 mg/min if there is no response with the lower dose. Continue to infuse until symptoms are controlled or until reaching a total dose of 10 mg. When there is high-output cardiac failure, be careful not to depress myocardial contractility to the point that cardiac failure worsens despite the slower heart rate.
-
Give propylthiouracil 200 to 400 mg PO/NG/PR followed by iodide 250 to 500 mg PO or IV 1 h after propylthiouracil. Aggressively search and treat the precipitating factor(s).
Myxedema Coma (Vol III—END/M3 Myxedema Coma)
Myxedema
coma occurs in chronically hypothyroid patients who are subjected to
stress. Exposure to a cold environment, pneumonia, and heart failure
are the most common stressors. When a history of hypothyroidism is not
available, diagnosis may be difficult. The characteristic thin hair,
puffy face, large tongue, and edematous skin may or may not be present.
Lab tests are not immediately helpful.
Myxedema coma is more common in women than in men, and half of the
patients are between the ages of 60 and 70 years. Hypothermia is a
common finding. Core temperature may be 29.5ºC (85ºF) or less.
Respiratory failure, hypotension, bradycardia, cardiomegaly, seizures,
coma, psychosis, paralytic ileus with acquired megacolon, and
dilutional hyponatremia may be present.
Because the diagnosis is often one of exclusion, attempt to correct each aspect of the patient’s problems using conventional therapies before administering thyroid hormone replacement.
Initial Management
-
Administer oxygen and protect the airway. Ventilate the patient if respiratory failure is present.
-
Administer hydrocortisone 100 mg IV to compensate for possible adrenal insufficiency.
-
Seizures due to hyponatremia can be terminated with 6 mL/kg of 3% NS solution.
-
Hypotension may be resistant to vasopressors, even when blood volume is expanded.
-
Re-warm the patient using non-invasive means.
-
When conventional measures fail to improve the patient, consider thyroid hormone replacement. The dose of thyroxine used can be fatal if given to a euthyroid patient. Give initial loading dose of L-T4 hormone 200 to 300 μg IV followed 24 hours later with a second dose (100 μg) IV.
-
Concomitantly, give L-T3 hormone 10 μg IV every 8 hours until the patient is stable and conscious.
-
Consult an endocrinologist regarding this dosing and subsequent doses.
O—OXYGEN, OPIATES, AND OTHER DRUGS OF ABUSE
Hypoxia
Always
consider hypoxia in the comatose or stuporous patient. Oxygen
administration should be an automatic response. Oxygen saturation
monitoring is an invaluable aid in identifying the hypoxic patient,
bearing in mind that oxygen saturation may be normal in patients
suffering from carbon monoxide poisoning. For a discussion of
respiratory failure, see Vol
III—Pathway 6 Adult Respiratory, Pathway 7
Pediatric Respiratory.
High Altitude Illness
High
altitude illness includes acute mountain sickness, high altitude
pulmonary edema, high altitude cerebral edema, transient cortical
blindness, and high altitude edema. (Vol
III—ENV5 High Altitude Illness)
Opiate/Heroin/Narcotic Overdose (Vol III—TOX12 Narcotic Overdose)
Opiate/heroin/narcotic
overdose patients exhibit constricted pupils, coma or stupor, and
respiratory depression. Needle tracks are usually present on the
forearms of chronic abusers.
Initial Management
-
If the patient needs resuscitative measures (such as airway management or IVs), do these before administering naloxone.
-
Give naloxone 2 mg IV, IM, or transtracheally. Naloxone may precipitate withdrawal, so restrain the patient prior to administration.
-
The duration of action of naloxone is only about 2 hours, so administer the long-acting opioid antagonist nalmefene 0.5 to 1.0 mg IV to keep the patient awake until the heroin is metabolized.
Cocaine Ingestion (Vol III—TOX 11 Cocaine Ingestion)
Cocaine
ingestion produces mental status changes, pulmonary edema, tachycardia,
hypertension, and hyperthermia. You may also observe mydriasis and
diaphoresis. Coronary artery vasoconstriction may result in myocardial
ischemia and infarction. Dysrhythmias are common. Intracranial
hemorrhage and seizures are sometimes seen. Rhabdomyolysis may result
in acute renal failure.
Initial Management
-
Administer oxygen and protect the airway if needed. ET intubation may be required. Be wary of using succinylcholine because of possible potassium release, secondary rhabdomyolysis.
-
Volume loading with NS restores normal blood volume and increases urine output, protecting the kidneys from damage secondary to the rhabdomyolysis. If the urine does not clear rapidly, add sodium bicarbonate at 1 mg/kg IV to alkalinize the urine.
-
Treat hypertension and tachycardia with diazepam, 5 to 10 mg IV, titrated for effect. Diazepam at a dose of 10 to 20 mg IV may also be used to terminate seizures.
Amphetamine Intoxication
Amphetamine
intoxication results in the same clinical picture as does cocaine
intoxication. The toxic effects are virtually the same, so follow the
guidelines listed for cocaine. (Vol
III—TOX 11 Cocaine Ingestion)
Phencyclidine Intoxication
Phencyclidine
(PCP) intoxication produces frightening and threatening hallucinations.
Agitation and violent behavior are major problems. Vertical and
horizontal nystagmus is common. Seizures, coma, muscle rigidity,
hypertension, rhabdomyolysis, and hyperthermia are present in severe
cases. Treat these problems as described for cocaine intoxication. (Vol
III—TOX 11 Cocaine Ingestion)
Initial Management
-
Administer oxygen and, if necessary, use RSI (Vol II—Air Skills 4 Rapid Sequence Intubation) to obtain oral tracheal airway. Avoid the use of succinylcholine if rhabdomyolysis is probable.
-
Use diazepam 5 to 10 mg IV or lorazepam 1 to 2 mg IV to sedate the patient. If this fails, use haloperidol 5 mg IM or IV. (Give benztropine [Cogentin] 1 to 4 mg PO with haloperidol.)
U—UREMIA AND OTHER METABOLIC ABNORMALITIES
Acute Renal Failure
Acute
renal failure results in coma if a rapid rise in BUN causes an increase
in serum osmolality. The brain is unable to adjust to this change.
Initial Management
-
Administer oxygen and protect the airway.
-
Always consider that the patient may have pre-renal failure secondary to hypovolemia. Clinically rule this out by history or examination. When in doubt, administer a fluid bolus to improve urine output and to correct metabolic abnormalities.
-
Hyperkalemia is a great danger and may result in cardiac dysrhythmia. This needs to be checked for and treated if present.
Electrolyte Abnormalities
Electrolyte
abnormalities such as hyponatremia, hypernatremia, hypercalcemia, and
hyperkalemia may be manifested as decreased level of consciousness.
These must be evaluated for and treated if present. (Vol
III—END/M7 Disorders of Electrilyte Concentration)
Acid-Base Abnormalities
Acid-base
abnormalities especially respiratory acidosis with hypercapnia may
result in decreased level of consciousness. This needs to be checked
for and treated if possible. (Vol
III—END/M6 Acid-Base)
Complete the thorough physical examination.
Caveats
No one can know everything about toxicology and critical care medicine. Consult early and freely with colleagues.
Do not start vasopressors for hypotension until the maximum effect of volume restoration has been achieved.
The keys to resuscitation are good airway management (Vol II—Air Skills 1 Aids to Intubation) and good blood volume management. (Vol III—Trau Care 2 Shock)
REFERENCES
-
U.S. Food and Drug Administration. FDA Drug Safety Communication: Serious medication errors from intravenous administration of nimodipine oral capsules. Available at http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm220386.htm
Accessed August 31, 2011.