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wikitox:2.1.11.4.2_antihistamines [2025/04/13 04:17] – ↷ Links adapted because of a move operation 191.53.156.184wikitox:2.1.11.4.2_antihistamines [2025/04/13 04:45] (current) – ↷ Links adapted because of a move operation 177.81.79.140
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 Seizures have been reported with most of these drugs, however the incidence is low except for pheniramine (incidence of seizures with pheniramine is approximately 30%). Seizures generally occur in association with other CNS signs, particularly delirium. Patients should be assessed on admission to see if they are hyperreflexic or have myoclonic jerks or any evidence of seizure activity.\\ Seizures have been reported with most of these drugs, however the incidence is low except for pheniramine (incidence of seizures with pheniramine is approximately 30%). Seizures generally occur in association with other CNS signs, particularly delirium. Patients should be assessed on admission to see if they are hyperreflexic or have myoclonic jerks or any evidence of seizure activity.\\
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-[[:wikitox:status_epilepticus_and_treatment_of_seizures|Seizures]] themselves are associated with an increased mortality. The acidosis produced by the seizures causes a subsequent further increase in the free drug concentrations by changing binding to the Na+ channel and plasma proteins. The increased concentrations may then lead to cardiac arrhythmias. In addition, acidosis affects the [[:concepts_systemic_alkalinisation|partitioning of basic drugs]] between the cell membrane and the Na+ channel binding site and increases Na+ channel blockade.+[[:wikitox:status_epilepticus_and_treatment_of_seizures|Seizures]] themselves are associated with an increased mortality. The acidosis produced by the seizures causes a subsequent further increase in the free drug concentrations by changing binding to the Na+ channel and plasma proteins. The increased concentrations may then lead to cardiac arrhythmias. In addition, acidosis affects the [[:concept_serum_alkalinization|partitioning of basic drugs]] between the cell membrane and the Na+ channel binding site and increases Na+ channel blockade.
  
 ==== Gastrointestinal effects ==== ==== Gastrointestinal effects ====
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 **Seizures** \\ Initially, [[:wikitox:benzodiazepines|diazepam]] 5-20 mg IV followed by [[:wikitox:barbiturates|phenobarbitone]] 15-18 mg/kg IV and elective intubation and ventilation. If neuromuscular blockade is required for management, EEG monitoring is mandatory. \\ **Seizures** \\ Initially, [[:wikitox:benzodiazepines|diazepam]] 5-20 mg IV followed by [[:wikitox:barbiturates|phenobarbitone]] 15-18 mg/kg IV and elective intubation and ventilation. If neuromuscular blockade is required for management, EEG monitoring is mandatory. \\
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-**Anticholinergic delirium** \\ Mild delirium can often be managed with reassurance plus or minus benzodiazepines. Severe hallucinations may require treatment with haloperidol. Although physostigmine is effective, the short half-life of this drug and its occasional life threatening adverse effects limit its application to diagnosis in delirium of unknown cause in patients with a normal ECG (and occasionally to facilitate gastrointestinal decontamination). General measures to manage delirium should be followed. \\  \\ **Arrhythmias** \\ It is often very difficult to distinguish whether the patient is having a supraventricular arrhythmia with aberrant conduction or primary ventricular tachycardia. Most arrhythmias, especially if they are associated with low output are treated in a standard cardiac arrest protocol manner. The main difference is the expected benefit from early and large doses of [[:concepts_systemic_alkalinisation|NaHCO3]]. All other treatments are of questionable efficacy and safety and therefore controversial. \\+**Anticholinergic delirium** \\ Mild delirium can often be managed with reassurance plus or minus benzodiazepines. Severe hallucinations may require treatment with haloperidol. Although physostigmine is effective, the short half-life of this drug and its occasional life threatening adverse effects limit its application to diagnosis in delirium of unknown cause in patients with a normal ECG (and occasionally to facilitate gastrointestinal decontamination). General measures to manage delirium should be followed. \\  \\ **Arrhythmias** \\ It is often very difficult to distinguish whether the patient is having a supraventricular arrhythmia with aberrant conduction or primary ventricular tachycardia. Most arrhythmias, especially if they are associated with low output are treated in a standard cardiac arrest protocol manner. The main difference is the expected benefit from early and large doses of [[:concept_serum_alkalinization|NaHCO3]]. All other treatments are of questionable efficacy and safety and therefore controversial. \\
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 **Alkalinisation** \\ Treatment with plasma alkalinisation to a pH of 7.5 using sodium bicarbonate (to alter both pH and sodium) or hyperventilation may be effective for antihistamine induced arrhythmias, extrapolating from TCAs. Initial treatment is normally with sufficient IV NaHCO<sub>3</sub>  to produce a pH of 7.5 to 7.55. Following the rapid correction of pH to 7.5 by IV NaHCO<sub>3</sub>, the patient is usually maintained at this pH by mild hyperventilation. \\  \\ Alkalosis may affect the partitioning of antihistamines between the cell membrane and the Na<sup>+</sup>   channel binding site and decrease Na<sup>+</sup>   channel blockade. \\  \\ **Further drug treatment** \\ All [[:wikitox:3.4.3.4_antiarrhythmics|class 1a antiarrhythmic]] drugs are contraindicated and lignocaine and [[:wikitox:2.1.11.2.1_phenytoin|phenytoin]] (class 1b drugs) while they may be used they may still exacerbate Na<sup>+</sup>   channel blockade and potentially exacerbate arrhythmias (e.g. convert VT into asystole). \\  \\ Magnesium is normally the drug of choice for treating torsade de pointes and is used for refractory arrhythmias in other settings. It may aggravate the hypotension and heart block. \\  \\ Second or third degree heart block should be treated with bicarbonate and isoprenaline followed by a pacemaker. \\  \\ **Hypotension** \\ This usually responds to volume expansion and pH correction. \\  \\ Refractory hypotension may require drugs with alpha agonist properties (e.g. adrenaline and noradrenaline) but these should be used cautiously, if at all, in this setting as they may precipitate ventricular tachycardia. **Alkalinisation** \\ Treatment with plasma alkalinisation to a pH of 7.5 using sodium bicarbonate (to alter both pH and sodium) or hyperventilation may be effective for antihistamine induced arrhythmias, extrapolating from TCAs. Initial treatment is normally with sufficient IV NaHCO<sub>3</sub>  to produce a pH of 7.5 to 7.55. Following the rapid correction of pH to 7.5 by IV NaHCO<sub>3</sub>, the patient is usually maintained at this pH by mild hyperventilation. \\  \\ Alkalosis may affect the partitioning of antihistamines between the cell membrane and the Na<sup>+</sup>   channel binding site and decrease Na<sup>+</sup>   channel blockade. \\  \\ **Further drug treatment** \\ All [[:wikitox:3.4.3.4_antiarrhythmics|class 1a antiarrhythmic]] drugs are contraindicated and lignocaine and [[:wikitox:2.1.11.2.1_phenytoin|phenytoin]] (class 1b drugs) while they may be used they may still exacerbate Na<sup>+</sup>   channel blockade and potentially exacerbate arrhythmias (e.g. convert VT into asystole). \\  \\ Magnesium is normally the drug of choice for treating torsade de pointes and is used for refractory arrhythmias in other settings. It may aggravate the hypotension and heart block. \\  \\ Second or third degree heart block should be treated with bicarbonate and isoprenaline followed by a pacemaker. \\  \\ **Hypotension** \\ This usually responds to volume expansion and pH correction. \\  \\ Refractory hypotension may require drugs with alpha agonist properties (e.g. adrenaline and noradrenaline) but these should be used cautiously, if at all, in this setting as they may precipitate ventricular tachycardia.