Dehydration and subsequent prerenal acute kidney injury can result when temperatures begin to rise in the summer months. As a result, medications with narrow therapeutic indices that are primarily renally excreted may accumulate. Here are the specific ones to look out for:
Pathophysiology: Angiotensin converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II. It also degrades bradykinin. Thus, ACE inhibitors have the effects of decreasing angiotensin II and increasing bradykinin. In the presence of ACE inhibition, bradykinin can accumulate and interact with vascular bradykinin B2 receptors, causing vasodilation, increased vascular permeability, increased c-GMP, and release of nitric oxide.
Treatment: Even though we generally treat with standard allergic reaction medications, none counteract the mechanism causing the problem. Steroids, H1-blockers, and H2-blockers should still be considered but may not alter the progression. Airway monitoring and management is paramount.
Several patients have recently presented with a medication history including tapentadol (Nucynta), the newest opioid formulation. It is approved for treatment of acute moderate-severe pain. Here are some key points:
Kiwi fruit and latex share several antigens in common. Thus, individuals who are allergic to either kiwi or latex may also suffer hypersensitivity reactions to the other material.
For patients with normal renal function, enoxaparin dosing for treatment of VTE is 1 mg/kg subcut every 12 hours OR 1.5 mg/kg subcut every 24 hours.
Studies have evaluated dosing for patients weighing up to 190 kg and found the 1 mg/kg q 12 hours dose to be safe and effective. It can even be used for patients heavier than 190 kg, but anti-Xa monitoring is recommended.
Several medications/chemicals can cause unique toxicologic reactions in pediatric patients.
Sulfamethoxazole (SMX)/trimethoprim (TMP) is the treatment of choice for PCP pneumonia. The IV formulation has been unavailable for almost a year due to shortage. It is contraindicated in patients with sulfa allergy. Here are the alternatives with adverse effects. You'll quickly see why pentamidine should generally be reserved for those with sulfa allergy and G6PD deficiency.
Mild-to-moderate disease:
Moderate-to-severe disease:
Adverse Effects:
Many consider Paracelsus (1493–1541) as the father of modern toxicology.
The introduction of the dose–response concept might have been his most important contribution to toxicology, meaning that everything is toxic at the right dose (even oxygen and water).
Many patients report an allergy to iodinated RCM, sometimes adding to the complexity of diagnostic decision making. Here are a few pearls to help:
Bottom line: Despite the lack of cross reactivity with shellfish/iodine allergies AND the very low risk associated with today’s low osmolality agents, premedication is still indicated in patient’s with a history of IHR to RCM.
The Rumack-Matthew nomogram is a well studied and validated tool to help assess the potential for liver toxicity following acute acetaminophen poisoning. Here is a brief review of when it is best utilized.
Outside-the-box situations:
Most cases of normal anion gap metabolic acidosis result from either urinary (RTA) or gastrointestinal HCO3- losses (diarrhea). A number of xenobiotics can also cause this disorder:
French LK, et al. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clinical Toxicology 2010;48:533–38.
Emerging evidence supports using intravenous fat emulsion (Intralipid) therapy for various drug overdoses, particularly those that are lipophilic. Within seconds to minutes of administration, toxic cardiovascular effects are reversed, including return of spontaneous circulation in cardiac arrest patients. Central nervous system effects also tend to improve.
Lipophilic agents for which there has been success include:
Bottom line: Consider intralipid therapy early in the course of a hemodynamically unstable patient with suspected overdose. Give a bolus of 1.5 mL/kg of 20% lipid emulsion over 1-2 minutes.
In the setting of acute cyanide poisoning, it is virtually impossible to obtain a timely cyanide level to help assess toxicity. However, there are two diagnostic tests that can help confirm your diagnosis.
Remember cyanide halts cellular respiration meaning the cells cannot utilize oxygen. Therefore, the venous PO2 should be about the same as the arterial PO2. The cells then switch to anaerobic metabolism, thereby producing lactate.
If benzodiazepines and supportive care fail to improve agitation and correct vital signs, several case reports indicate the successful use of cyproheptadine, an antihistamine with nonspecific antagonist effects at 5-HT1A and 5-HT2A receptors.
Cyproheptadine is available in 4 mg tablets or 2 mg/5 mL syrup. When administered as an antidote for serotonin syndrome, an initial dose of 8-12 mg is recommended, followed by 2 mg every two hours until clinical response is seen. Cyproheptadine is only available in an oral form, but it may be crushed and given through a nasogastric tube.
Cyproheptadine may lead to sedation, but this effect is consistent with the goals of management. It may also produce transient hypotension due to the reversal of serotonin-mediated increases in vascular tone. Such hypotension usually responds to IV fluids. Cyproheptadine is rated category B for safety in pregnancy by the FDA.
In a patient with toxin-induced bradycardia and hypotension, here is a quick differential to help identify the responsible substance:
Less commonly seen causes include: magnesium, propafenone, and plant toxins (aconitine, andromedotoxin, veratrine).
Physostigmine has been used extensively in the fields of anesthesiology and emergency medicine. The only use of physostigmine with sound scientific support is for the management of patients with an anticholinergic syndrome, particularly those without cardiovascular compromise who have an agitated delirium. In this population, physostigmine has an excellent risk-to-benefit profile.
We are all familiar with the classic ECG abnormalities caused by the sodium channel blocking properties of tricyclic antidepressants (QRS interval widening, R wave in aVR, S wave in I and aVL, and rightward deviation in terminal 40 msec of QRS). Here are some other medications that also block cardiac sodium channels in a similar manner:
Many drugs/toxins cause nystagmus, particularly in overdose. Vertical, horizontal, or rotary nystagmus may be noted.
The most common drug/toxin overdoses that cause nystagmus are the following:
According to the Food Allergy and Anaphylaxis Network, the eight most common food allergies, which account for 90% of the food allergies in the U.S., are: dairy, soy, wheat, shellfish, fish, peanut, tree nut, and egg.
Several medications are formulated with these ingredients and should be avoided in patients with reported allergies.