Acute Carbon Monoxide Poisoning: Emergency ...

5 downloads 6 Views 423KB Size Report
rebreather mask (NRM) and transported to UMC. From the Division of Emergency Medicine and the Hyperbaric. Medicine Service, University Medical Center, ...

Acute Carbon Monoxide Poisoning: Emergency Management and Hyperbaric Oxygen Therapy HARRY W. SEVERANCE, M.D.

J. C. KOLB, M.D.

F. B. CARLTON, M.D.

ROBERT C. JORDEN, M.D.

Jackson, Mississippi

of February 6-7, 1989, central Mississippi was among the areas suffering a crippling ice storm that interrupted electrical power to large segments of the population for periods up to one week. Many families and homes were inadequately prepared for alternative home heating and some resorted to open, unventilated fires in their homes. During the period from February 7-9, the University of Mississippi Medical Center (UMC) treated sixteen cases of carbon monoxide (CO) poisoning secondary to unventilated home fires or stormrelated damage to existing heating systems. Five cases were children with ages ranging from 11 months to 11 years. Eleven cases were in adults from 17 to 75 years old. Six of these cases resulted in hyperbaric oxygen (HBO) therapy; these cases are briefly reviewed. DURING THE PERIOD

Report of Cases Case 1: A 29-year-old female was using an unventilated charcoal grill inside her home for heating and cooking. The grill had been lit since the previous evening. The patient was found by family members unconscious and unresponsive. On arrival of paramedics, the patient was unresponsive and had the following vital signs (VS): P 116, BP 100/ 38, respirations (R) 12. Her airway was patent, though it was observed that she had vomited at least once. Smoke fumes were present in the house. The patient was placed on 100% oxygen (02) via nonrebreather mask (NRM) and transported to UMC. From the Division of Emergency Medicine and the Hyperbaric Medicine Service, University Medical Center, Jackson, MS.

OCTOBER 1989

An ice storm in February 1989 resulted in numerous incidences of carbon monoxide poisoning in central Mississippi secondary to exposure to open fires in unventilated living spaces. Sixteen cases were treated during this period at the University of Mississippi Medical Center and 6 received Hyperbaric Oxygen therapy. These 6 cases and the mechanisms of CO poisoning are discussed and recommendations for emergency management are reviewed.

After approximately 10 minutes on 0 2 the patient became responsive to verbal stimuli but remained lethargic, even after arrival to the hospital. Physical examination was unremarkable and there were no focal neurologic deficits. Initial arterial blood sampling on 100% 0 2 demonstrated a pH of 7.50, a pCO 2 of 27, a p0 2 of 316, and a carboxyhemoglobin (COHb) level of 22.2%. Because of lethargy after smoke inhalation the patient received a single HBO treatment of 2.4 atmospheres absolute (ATA) for 90 minutes. She tolerated this well and was entirely alert before the end of the procedure. She was eventually discharged from the emergency department after observation. Case 2: A 75-year-old female was using an unventilated charcoal grill to keep warm and cook. The patient became dizzy and complained of loss of vision as reported by family members who transported her to UMC. On arrival her VS were: P 88, 321

BP 110/70, and R 20. Physical examination including the neurologic examination was unremarkable. Initial room air arterial blood gases were: pH 7.40, p CO2 37, pO 2 60, and COHb 37.0%. Because of her smoke inhalation, age and past medical history which included diabetes and cardiac disease, HBO therapy was attempted. However, the patient was not able to tolerate the treatment as she could not equalize middle ear pressure and became claustrophobic. Therefore she was observed on 100% 0, NRM with serial arterial COHb monitoring. After 8 hours her COHb level had dropped to 5.4%. She developed no complications during observation and was eventually discharged home. Case 3: A 55-year-old female relative present in the same house as case 2 was transported to UMC after discovery of CO poisoning in her relative. The patient was awake and responsive at home but complained of dizziness and headache and one nearsyncopal episode. Arterial sampling on 100% 0 2 demonstrated a pH of 7.37, a PCO 2 of 40, a PO 2 of 467, and a COHb level of 26.4%. Because of her symptoms and history of smoke inhalation she received one treatment of HBO at 2.4 ATA for 90 minutes. Her symptoms resolved during treatment and after observation she was discharged home. Case 4: An 18-year-old female was brought to UMC by her boyfriend who reported finding her lethargic at home. Other family members were too weak to come to the hospital. All had complaints of dizziness, headache, vomiting and increasing lethargy. This patient denied any exposure to a source of combustion in the house. Later it was discovered that the house had central gas heating that had sustained ice-storm related damage. The patient was arousable but very lethargic, with an otherwise normal physical and neurologic examination. Her vital signs were normal. Because of a history of symptoms affecting several patients simultaneously CO poisoning was suspected and arterial blood gases obtained. Room air arterial blood gases showed the following: pH 7.37, PCO 2 36, PO 2 117, and COHb 30.5%. The patient was immediately placed on 100% 0 2 via NRM. Because of her elevated COHb level with symptoms, she received one HBO treatment at 2.4 ATA for 90 minutes with complete resolution of symptoms. After observation she was discharged home. Case 5: The 50-year-old mother of the above patient (case 4) was brought to UMC after discovery of CO poisoning in the daughter. The mother's complaints and physical examination were similar to those of her daughter except she was less lethargic. Arterial sampling done while 100% 0 2 was being 32 2

established returned as follows: pH 7.35, PCO 2 42, PO 2 56, COHb 29.2%. Because of her COHb level and presence of symptoms she was treated with one HBO treatment at 2.4 ATA for 90 minutes. Her symptoms resolved and after observation she was discharged home. Case 6: A 17-year-old male in the same house as cases 4 and 5 was brought to UMC concurrently with patient 5. The patient was found lying in bed at home arousable but complaining of weakness and dizziness. Physical and neurologic examinations were unremarkable and arterial sampling on 100% 0 2 via NRM were: pH 7.40, PCO 2 40, PO2 417, COHb 27.8%. Because of his symptoms and COHb level he was given one HBO treatment at 2.4 ATA for 90 minutes with resolution of his symptoms. After observation he was discharged home. Discussion Pathophysiology: Poisoning from CO occurs from the inhalation of the products of incomplete combustion of carbonaceous compounds. The usual sources are automobile exhaust, gas or kerosene heaters and stoves and open, unventilated fires in closed spaces.' CO binds to the hemoglobin molecule with an affinity 230-270 times greater than that of oxygen and forms COHb which can be expressed as a percentage of hemoglobin saturation . 2 CO poisoning is the direct cause or a contributing factor in 80% of fatalities occurring within 12 hours of injury in fire victims. 3 In 30% it is the sole factor in their failure to escape. The pathophysiology of CO poisoning is not entirely elucidated but may involve at least four different, mechanisms. Competitive displacement by CO of 02 off the Hb binding sites 1,2 leads to impaired 02 transport and tissue hypoxia.' Tighter binding of remaining Hb bound 02 results in a shift of the oxygen hemoglobin dissociation curve to the left with resultant decreased 1,2,4 02 unloading at the tissues and further hypoxia.' • Cardiac output is decreased as tissue oxygen perfusion decreases and also possibly as CO binds to cardiac myoglobin further decreasing 02 perfusion of cardiac muscle. I CO also binds to the cytochrome chain, primarily cytochromes Aa3 and P 450 with possible poisoning of cytochrome function. It is at this micro-cellular level where many damaging effects of CO poisoning are postulated to occur.' a Clinical Presentation: Clinically, CO poisoning can present non-specifically with a multitude of symptoms that often roughly equate with arterial COHb levels. Complaints suggestive of mild CO poisoning, such as headache and irritability may appear with levels as low as 5-10%. Between 10JOURNAL MSMA



I

II

111

Seizures Significant neurologic deficit Coma or history of loss of consciousness (including syncope) Myocardial ischemia (clinical or ECG) Significant metabolic acidosis (pH < 7.32) Smoke inhalation (i.e. possible cyanide exposure) with CO level > 20%

CO > 30%

CO < 30%

HBO + Hospitalization

HBO therapy

1 00% 02 x 4 hr

1

No symptoms

Nausea, vomiting, headache, dizziness, weakness, visual blurring, confusion, mild neurologic deficits, or abnormal psychometrics

1

Sx resolved

Hospitalization x 24 hr for observation

CO > 10% or history of exposure 100% 02 x 4 hr

1

Sx persistent

Sx resolved

Repeat HBO therapy

Discharged if CO < 5% follow-up with private MD

Discharge if CO level < 5% follow-up with private MD

Sx persistent

Consider HBO

Figure 1. Reproduced by permission from Emergency Medicine: Concepts and Clinical Practice, 1988. 20% one may see worsening headache, errors in judgement, nausea and vomiting, dizziness and tachycardia. Between 20-40%, increasing lethargy and alterations in mentation can occur. At levels greater than 40%, severe symptoms such as cardiac dysrhythmias, angina, seizures, coma and death can be encountered. Other factors can influence presenting symptoms. These include the patient's age and physical health, length of exposure and time since exposure and activity level during exposure. Also, the source of the exposure can affect symptoms; for example, victims of smoke inhalation are more symptomatic at lower COHb levels. This may be due to the presence of other toxins, such as cyanide. Cutaneous manifestations which may be seen at any COHb level include an erythema-like rash, edema, blisters and bullae . 6 The classic "cherryred" skin is usually only seen in terminal cases. Complications of CO poisoning include: cardiac dysrhythmias, myocardial ischemia, metabolic acidosis, pulmonary edema and/or hemorrhage, rhabdomyolysis and renal failure, neuropsychiatric changes such as alterations in mentation, gait, skill performance, and mood. Pulmonary and renal comOCTOBER 1989

C. V.

Mosby Co.,

plications may not be recognized until hours after the initial insult. Neuropsychiatric complication may begin days to weeks after the acute event.'' 8 Laboratory tests are of some help in evaluation of CO poisoning. The hallmark finding is an elevated arterial COHb level, though the level may not always be compatible with the patient's symptoms. ABG's may appear normal as many, or nearly all, facilities measure 0 2 dissolved in plasma, not hemoglobinbound oxygen. Also, if oxygen saturation is computed rather than measured, a falsely normal value will be reported despite a significant CO poisoning. There is often an anion gap acidosis present in these patients due to lactic acidemia from tissue hypoxia. Creatine phosphokinase (CK) can be elevated, especially the MB and MM bands. Free hemoglobin and myoglobin may be noted in the urine and may equate with decreasing renal function. Ischemic changes may appear on ECG and dysrhythmias may be seen on cardiac monitors. Serial chest radiographs may demonstrate evolving changes of pulmonary edema, especially in cases of smoke inhalation. Treatment: All patients should be immediately 323



or burns should be ruled out during a quick primary survey. During initial stabilization all patients should have ABG's with an arterial COHb level. If the COHb level is significantly elevated, the following additional tests should be obtained: CBC, electrolyte screen, serum CK level with isoenzymes and urine hemoglobin and myoglobin determinations. These patients should receive continuous cardiac monitoring upon arrival and a baseline ECG as well as initial and follow-up chest radiographs. After initial stabilization and interventions are completed a thorough secondary survey including a careful baseline neurologic examination should be conducted.

removed from the source of CO poisoning and have 100% oxygen administered. It is important to remember that CO is competitively bound to Hb. The half-life for displacement of CO from Hb at 21 % F10 2 is 4-5 hours. With 100% 0 2 the time is reduced to 90 minutes and at 2.4 - 3.0 ATA the time is reduced to 20-30 minutes. The administration of oxygen not only reduces the bound half-life of COHb, but shortens the acute symptoms of CO intoxication. Therefore, all patients should be treated with at least 100% oxygen until all acute symptoms resolve. Upon arrival at the emergency department airway, breathing and circulation should be reassessed and stabilized. Other injuries such as trauma

H.B.O Chamber Not Available Locally 1

>40% Referral to H.B.O. Center

CO Level

1

None or only headache

I

25% Treat with H.B.O.

CO Level ∎

1 None or only headache

Suggest Documents