Intoxication With Central Nervous System Depressant Agents

89 Intoxication With Central Nervous System Depressant Agents

Claudia Analía González ¹, Roxana Andrea Bertrand ¹

¹ Unit of Toxicology and Pharmacovigilance. Hospital Municipal de Agudos “Dr. Leónidas Lucero”, Bahía Blanca, Argentina

89.1 Introduction

Patients with CNS depressant intoxication often constitute a toxicological emergency. The most common cause of intoxication in adults is attempted suicide, followed by accidental causes, mainly in children.

Given the severity of the emergency that this type of drug can cause, it is critical to correctly evaluate the problem, with adequate patient interview, physical examination and complementary methods. The aim is to reach a presumptive diagnosis, understanding the most likely etiology and start specific treatments immediately.

This chapter provides a practical guide to the management of patients entering an emergency department intoxicated with central nervous system (CNS) depressant agents.

89.2 Development

When patients with altered state of consciousness enter the emergency department, we should always consider possible exposure to CNS depressant agents because this condition requires rapid diagnosis and treatment.

Many various drugs have CNS depressant activity (Table 89.1); therefore, family history of the patient is extremely relevant because it can yield data on the medication administered to the patients, their availability, and so on. All these aspects are useful in the analysis of intoxication cases (Table 89.2).

Alcohol
Benzodiazepines
Barbiturates
Opioids
Phenothiazines
Butyrophenones
Anticonvulsants
Tricyclic antidepressants
Others
Antihypertensives (beta-blockers)
Calcium channel blockers
Digitalis
Vinyl chloride
Methaqualone
Chloral hydrate

Table 89.1. Main drugs with CNS depressant activity.

Questions	Answers
What did you take?	Identification of the generic name of the substance involved, the composition of the product containing it, and its presentation
How much did you take?	Evaluates the extent of intoxication in order to start immediately the appropriate treatment
When?	It’s the latency time: the time of ingestion to the time patient presents at hospital or onset of symptoms
How?	Evaluates the administration route of the poison
Where?	Know where it happened (it helps when you do not know what the patient has taken)
Why?	To better understand the intoxication

Table 89.2. Questions for the diagnosis of intoxication.

Few signs and symptoms are special features and, on the contrary, are often similar to those presented by other diseases such as infectious disease, stroke, coma, etc. A thorough physical examination is essential to search for meaningful data (Table 89.3).

Clinical features	Suspected substance
Miosis, bradycardia, nystagmus, ataxia, coma, hypoglycemia, hypothermia, ethyl breath	Alcohol
Muscle hypotonia, drowsiness, stupor, coma, seizures, cardiorespiratory depression, hyporeflexia, ataxia, hypothermia	Benzodiazepins
Nystagmus, somnolence, cardiorespiratory depression, hypotension, slurred speech, hypotonia, ataxia, dysarthria, hypothermia, miosis, flaccid coma	Barbiturates
Sensory depression, bradypnoea, coma, seizures, spasticity, hyperreflexia, bradycardia, constipation, hypotension, hypothermia, miosis	Opioids
Arrhythmias, hypotension, hypothermia, sensory impairment, oculocephalic crisis spasmodic torticollis, hypertonia, myoclonus, ataxia, orolingual dyskinesia	Phenothiazines
Convulsions, sensory depression, extrapyramidal symptoms, anticholinergic symptoms, arrhythmias, hypotension, hypothermia	Butyrophenones
Hypotension, hypothermia, tremor, hyperreflexia, dysarthria, coma, convulsions, sensory depression, anticholinergic symptoms, arrhythmias	Tricyclic antidepressants
Nausea, vomiting, myoclonus, mydriasis dysarthria, nystagmus, ataxia, diplopia, blurred vision, respiratory depression	Carbamazepine	Anticonvulsants
Arrhythmias, hypotension, nausea, vomiting, seizures, tremors, nystagmus, vertigo, mydriasis, dysarthria mental confusion, ataxia diplopia, blurred vision	Phenytoin

Table 89.3. Clinical signs of CNS depressant intoxication.

Toxicological screenings are limited and not always available in all emergency departments; therefore, available laboratory tests should be performed, such as acid-base status, electrolytes, glucose, urea, white blood cell count, hematocrit, creatine, lactic acid, anion gap, and urine sediment.

The electrocardiogram (ECG) is an inexpensive, quick means to obtain objective information on intoxication etiology and severity. Rarely will ECG alone provide guidance to establish a precise etiologic diagnosis; however, together with findings from history, epidemiology, vital signs, characteristics of the skin, eyes and peristalsis, the ECG has a fundamental diagnostic value. CNS depressants can cause rhythm disturbances in cardiac conduction, often with PR interval prolongation, QRS widening, QT prolongation, and atrial and ventricular arrhythmias.

The physical examination will disclose signs that can help in the diagnosis: vital functions (blood pressure, heart rate, pulse), skin and mucosa colour, smell of the expired air and the vomit or clothes, body temperature, and breathing pattern.

Patients intoxicated with CNS depressants may have different levels of altered consciousness. This is of great clinical importance, because it represents the key point to understand whether the clinical features are related to a structural cause (stroke or subdural hematoma) or to a toxic/metabolic cause (intake of psychiatric drugs, opioids, hydrocarbons, alcohol, hyperosmolar coma). Therefore, a quick and easy way to orient toward the etiology is to analyze three parameters: pupils, equal and reactive to light; eye position at rest and response to challenging manoeuvres; motor response to painful stimuli. In disorders caused by CNS depressants the first function affected is usually breathing followed by pupillary reflexes. In contrast, pupillary reflexes are altered earlier when the disorder is due to a structural cause (Table 89.4).

Manifestations	Toxic/metabolic coma	Structural coma
Pupils	Not modified	Modified
Oculocephalic manoeuvre	Maintained	Altered
Papilledema	Rare	Frequent
Motor system	Usually not compromised	Usually compromised
Vital signs	Highly altered	Not highly altered

Table 89.4. Differences between “structural” and “toxic/metabolic” manifestations of coma.

89.3 Treatment of the Most Frequent Types of Intoxication With CNS Depressants

Prompt treatment of clinical picture caused by the toxic agent and successful patient management are key to management. Evaluation will follow the ABCD scheme:

Only gold members can continue reading. Log In or Register to continue