Pediatric Calcium Channel Blocker Toxicity Clinical Presentation

Whenever a patient presents with bradycardia, hypotension, and an altered mental status, gather a short and AMPLE (ie, allergies, medications, past medical history, last meal, and events of the incident) medical history.

If the patient ingested medications, ascertain type, dose, and number or amount. Determine the number of tablets that are missing from the bottle of medicine ingested by the patient. If the number of pills in the bottle at the time of the ingestion is unknown, determine the number of pills that the bottle initially contained (ie, the maximum number of pills the child could have taken).

Ascertain whether the ingestion is a sustained-release preparation. Ask the patient's family members what medications they are taking, because these are most likely the substances that the patient ingested.

Finally, try to determine the time between the ingestion and presentation to the emergency department (ED), because this interval provides an indication of how long the pharmaceuticals have had to be absorbed in the patient's digestive system.

If a suicide attempt is suspected, try to determine whether other medications or alcohol could have been co-ingested. Acetaminophen or aspirin ingestion is especially important to determine because both have known medical treatment modalities.

When calcium channel blocker ingestion is suspected, specifically question the patient or family about cardiac or pulmonary manifestations of calcium channel blocker toxicity.

Other questions to answer include the following:

• Did the patient exhibit chest pain, diaphoresis, flushing, palpitations, weakness, peripheral edema, dyspnea, or cough
• Does the patient exhibit any signs of CNS involvement
• Does the patient have a history of drowsiness, confusion, seizure, dizziness, headache, tremor, nausea, vomiting, or syncope

Pay particular attention to the cardiac, vascular, and neurologic examinations because calcium channel blocker toxicity manifests most physical findings in these systems. According to one study, maximal elapsed time to onset of symptoms ranged from 3 hours (seen with normal preparations) to 14 hours (in the setting of sustained-release medications).^[4] These onset times should be considered when discharging patients home who may or may not have ingested calcium channel blockers.

Begin the physical examination of the patient who has ingested an unknown amount of a calcium channel blocker by checking vital signs. The heart rate may be decreased if the sinoatrial (SA) node is poisoned or may be increased if the patient is experiencing reflex tachycardia secondary to peripheral vasodilation and hypotension. Hypotension may last up to 24 hours with some sustained-release, long-acting medications.

When examining the head, eyes, ears, nose, and throat, ensure that the patient's pupils are equal, round, reactive to light, and not pinpoint. Specifically look for signs of focal neurologic deficits.

A detailed, 6-part neurologic examination should be performed, and the findings should be documented. With the exception of nimodipine, calcium channel blockers have poor CNS penetration. Therefore, drowsiness, seizures, or altered mental status in the absence of hemodynamic collapse should alert the physician to the possibility of co-ingestions.

Examine the abdomen, paying particularly close attention to the right upper quadrant. With calcium channel blocker toxicity, venous congestion can lead to hepatic engorgement and stretching of the hepatic capsule, causing hepatic tenderness and hepatomegaly. Hepatojugular reflux may also be observed. Listen for bowel sounds because calcium channel blockers may cause enteric dysmotility. Bowel perforation secondary to calcium channel blocker ingestions has been reported. Peritoneal signs of rebound and guarding are ominous findings.

Hyperglycemia may result from impaired insulin release in addition to insulin resistance. Although beta-antagonist toxicity may resemble calcium channel blocker toxicity in most aspects of the physical examination, the serum glucose level may help to identify which cardiovascular toxin was ingested, because beta antagonists often lower the glucose level.

Levine et al retrospectively analyzed 40 nondihydropyridine overdoses and found that the severity of toxicity correlated directly with the degree of hyperglycemia. For patients requiring temporary pacemaker placement or vasopressor support compared with those who did not, median initial serum glucose concentrations were 188 mg/dL (interquartile range, 143.5-270.5 mg/dL) and 129 mg/dL (98.5-156.6 mg/dL), respectively. The median peak serum glucose concentrations for those 2 groups were 364 mg/dL (267.5-408.5 mg/dL) and 145 mg/dL (107.5-160.5 mg/dL).^[5]