Medic 49 was called to a wooded area near a private residence for a missing person and concern for overdose. Police were already on scene and had walked approximately 0.5 miles into the wooded area behind the home where they found a 30-year-old female unresponsive with several pill bottles nearby. The family, who had reported the patient missing, stated that the patient had a history of suicidal thoughts.
On EMS arrival, the patient was still unresponsive and hypoxic with an oxygen saturation of 76% on RA. The patient was also tachycardic to 130 and had an initial blood pressure of 140/90. The patient was not moving spontaneously and did not localize to painful stimuli. She would moan spontaneously, but was not speaking in words or sentences. A bag valve mask (BVM) was applied and the patient was provided with positive pressure breaths. She was carried out of the woods on a Reeve’s with no evidence of trauma. Police took the empty pill bottle near the patient.
The patient was placed in the ambulance and taken to a nearby hospital. En route, the patient became hypotensive to 80/40 with improved oxygen saturation with BVM to 89% and she remained tachycardic. Shortly before arrival to the hospital, the patient had no palpable pulse and CPR was started. A right tibial intraosseous (IO) access was initiated. She received 1mg of epinephrine and was noted to be in pulseless electrical activity (PEA) arrest.
On arrival to the hospital, the patient remained in PEA. She received CPR and more epinephrine. Initially, the medications the patient took were unknown, but EMS called detectives who stated the patient had likely taken amitriptyline and baclofen. Her prescription had just been filled three days prior and the bottles were empty. With this information, the patient also received 2 amps of bicarbonate and intralipid.
A pulse was regained and the patient was intubated for continued hypoxia. After ROSC, the patient was still hypotensive and tachycardic. She received intravenous fluids (IVF). An ECG was performed (see Figure 1, above) so the patient was placed on a bicarbonate infusion. Given her continued hypotension, central venous and arterial catheters were placed and the patient was started on norepinephrine, which improved her blood pressure to the 100s/60s with a heart rate of 100. The patient was placed on propofol and fentanyl for sedation and analgesia, but she had no purposeful movements so was deemed to be a hypothermia protocol candidate. She was also determined to be a good candidate for care in the tertiary care center medical intensive care unit (MICU), so a local helicopter service was called to transport her and she was taken to head CT as part of standard hypothermia protocol. The patient had no evidence of intracranial hemorrhage. The helicopter arrived and transported the patient to the tertiary care center.
While in the MICU, the patient remained unresponsive for six days. She did receive hypothermia protocol. She received several brain death examinations, but given that she had a cardiac arrest from overdose, the patient was given more time to metabolize all drugs. On day six of hospitalization, the patient opened her eyes and began following commands. She was extubated and was awake, alert and oriented, and still endorsing suicidal ideation with no specific plan. The patient was evaluated by psychiatry and deemed to be a candidate for inpatient psychiatric treatment.
On hospital day 10, the patient was transferred to the inpatient psychiatric department in stable condition. She had some residual short-term memory loss, but otherwise had no other focal neurologic deficits on exam.
Overall, 2.9 percent of the adult population attempts suicide1 and the suicide rate in the general population over a lifetime of 70 years is approximately one percent.2 Studies of suicide attempters suggest that 1% to 2% complete suicide within a year after the initial attempt, with another 1% committing suicide in each following year.3 In the 25-to-34-year-old age group, suicide is the second leading cause of death.4 There are several risk factors for suicide attempt:4
- Family history of suicide
- Family history of child maltreatment
- Previous suicide attempt(s)
- History of mental disorders, particularly clinical depression
- History of alcohol and substance abuse
- Feelings of hopelessness
- Impulsive or aggressive tendencies
- Cultural and religious beliefs (e.g., belief that suicide is noble resolution of a personal dilemma)
- Local epidemics of suicide
- Isolation, a feeling of being cut off from other people
- Barriers to accessing mental health treatment
- Loss (relational, social, work, or financial)
- Physical illness
- Easy access to lethal methods
- Unwillingness to seek help because of the stigma attached to mental health and substance abuse disorders or to suicidal thoughts
Tricyclic antidepressants (TCAs) continue to play a role in the treatment of enuresis, obsessive-compulsive disorder, attention deficit hyperactivity disorder, school phobia and separation anxiety in the pediatric population. In adults, indications for TCAs include depression, neuralgic pain, chronic pain and migraine prophylaxis. Some of the more commonly prescribed TCAs are:5
In the 2014 American Association of Poison Control Centers’ National Poison Data System Annual report, TCAs accounted for 4,418 single exposures and 12 deaths. The TCA most frequently ingested was amitriptyline.6 Fatality before reaching a healthcare facility occurs in approximately 70% of patients attempting suicide. Only 2–3% of TCA overdose cases that reach a healthcare facility result in death. Cyclic antidepressant (CA) toxicity occurs in both men and women. However, the incidence of CA exposure is greater in women than in men because women are at a higher risk for suicide attempt. CA toxicity occurs at all ages. The incidence of TCA toxicity is most prevalent in individuals 20–29 years old.5
Mechanism & Toxicity
TCAs have long half-lives that generally exceed 24 hours. After the TCAs are metabolized in the liver they are then excreted through the kidneys.5
TCAs have effects due to several mechanisms. First, they inhibit norepinephrine and serotonin re-uptake at nerve terminals. These medications can enter the central nervous system, which allows for both therapeutic and toxic effects seen with TCA use and overdose. Second, TCAs have some anticholinergic action.5 A good way to remember anticholinergic toxidrome is the following: “Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone.”
Anticholinergic effects of TCAs include: 5
- Blurred vision
- Decreased bowel sounds
- Dry skin
- Memory loss
- Mydriasis (dilated pupils)
- Urinary retention
- Altered mental status
Third, TCAs block certain cardiac sodium channels. Overdose on these medications can lead to disruption of the cardiac conduction system. TCAs, function similarly to the class Ia antiarrhythmics (quinidine, procainamide, disopyramide). Sodium flow through the fast sodium channels is decreased leading to a widened QRS complex. TCAs also likely have direct effect on myocardial contractility leading to hypotension.5
ECGs should routinely be performed in patients presenting with concern for overdose. There are several characteristic findings in TCA overdose on ECG. First, patients will have an interventricular conduction delay with a QRS greater than 100 ms. A right axis deviation with a terminal R wave in aVR may also be observed. Patients will also likely have sinus tachycardia.7 The QRS duration seen on ECG can also be predictive of seizures (QRS > 100ms). 7
In the obtunded patient, respiratory support should be provided according to local protocols. IV or IO access should also be obtained. Patient should be transported to the nearest appropriate emergency department for further diagnosis, treatment and consultation with a poison control center. Vomiting should not be induced, and administration of activated charcoal remains controversial and should not delay transport. For patients with a QRS > 100ms, sodium bicarbonate may be administered if included in local protocols. For seizures, benzodiazepines should be administered.8
Baclofen is primarily used to treat spasticity and it does not produce euphoria and does not possess addictive properties. However, baclofen does have some sedative and anxiolytic effects. There are few cases of baclofen being used as a drug of abuse, but baclofen overdose for suicide attempts has been described.9
Mechanism & Toxicity
Baclofen is a central nervous system depressant and functions as a skeletal muscle relaxant. Overdose symptoms are:10
- Respiratory depression
Several cases have been presented that show that baclofen overdose can mimic signs and symptoms of brain death for an extended period of time with patients who go on to have good neurologic outcomes.11 As was seen with our patient, even with decreased responsiveness and poor initial neurologic exam, baclofen overdoses can have good neurologic outcomes.
Treatment for baclofen is primarily supportive. There should also be an investigation for possible co-ingestions. Advanced respiratory support may be required in obtunded patients. If seizures occur, benzodiazepines can be administered. Activated charcoal can be considered if there is known recent ingestion and the patient is able to safely protect their airway. Administration should not delay transport and crews should follow local protocols.
In this case, we present a patient with polysubstance overdose. Early recognition of the substances ingested allows for appropriate treatment of patients can be life-saving. Airway, breathing and circulation should be supported as necessary in overdose patients and further treatment should occur based on local protocols.
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11. Sullivan R, Hodgman M, Kao L, et. al. Baclofen overdose mimicking brain death. Clinical Toxicology. 2012;50(2):141–144.