Thursday, November 6, 2014

Malaria - Quick review

Although Ebola has been all the furor in the recent weeks, fever in travelers is NOT Ebola most of the times. Depending on the region and season, the usual culprits are more likely than Ebola, these include malaria, dengue, yellow fever, chikungunia virus, hepatitis, salmonella and other intestinal bugs, multiple parasites among others. Here is the Q&A for malaria and babesia from this month's NEJM.

What is the annual incidence of malaria in the United States?
In the United States, the annual incidence of malaria is approximately 1500 cases. In 2010, a total of 1691 cases were reported to the Centers for Disease Control and Prevention (CDC), the largest number reported since 1980; P. falciparum, P. vivax, P. malariae, and P. ovale were identified in 58%, 19%, 2%, and 2% of cases, respectively.

How do malaria and babesiosis differ in appearance on a peripheral blood smear?
Intraerythrocytic parasites are seen in both malaria and babesiosis. Plasmodia metabolize heme to form an intracellular crystallized pigment, hemozoin. Although hemozoin is not invariably identified in cases of malaria, its presence reliably distinguishes malaria infection from babesia infection. Malaria parasites can be distinguished from B. [Babesia] microti by the presence of recognizable gametocytes (characteristically banana-shaped in Plasmodium falciparum and round, with a granular appearance, in nonfalciparum species). In addition, intracellular vacuoles and extracellular merozoites are unusual in malaria but common in babesiosis, and the classic “Maltese cross” (a tetrad of parasites budding at right angles) is unique to babesia species.

Which malaria species can remain dormant in the liver?
In the case of P. vivax and P. ovale, some sporozoites (immature malaria parasites) do not replicate immediately when they invade hepatocytes but remain dormant (as hypnozoites) for prolonged periods. The average time to relapse is approximately 9 months, but it can range from weeks to years. The interval to relapse depends on the strain (earlier with tropical strains and later with temperate strains), the initial inoculum, and host factors (e.g., febrile illnesses can trigger relapse associated with P. vivax). None of the commonly used prophylactic agents (chloroquine, mefloquine, doxycycline, or atovaquone–proguanil) eliminate hypnozoites. Primaquine, the only effective drug against dormant hypnozoites, has not been approved by the Food and Drug Administration for primary prophylaxis, but the CDC endorses its use for prophylaxis in Latin American countries where P. vivax predominates, because the drug can prevent both primary attacks and relapses caused by all species that are a source of malarial infection.

How is acute or recurrent P. vivax infection treated?
In patients with acute or recurrent malaria infection, treatment depends on the species and the resistance status in the area where the infection was acquired. P. falciparum is resistant to chloroquine in most regions in which it is endemic and resistant to mefloquine in parts of Southeast Asia. In contrast, nonfalciparum malaria parasites do not have substantial resistance to mefloquine, and the distribution of chloroquine-resistant P. vivax malaria is limited, occurring primarily in Indonesia and Papua New Guinea. After treatment is initiated, peripheral-blood smears should be obtained daily for 4 days (parasitemia is typically eliminated by day 4), on days 7 and 28 to confirm eradication, and at any time symptoms recur, suggesting treatment failure. In areas other than those with known chloroquine resistance, chloroquine, followed by a 14-day course of primaquine to prevent subsequent relapses, remains the standard treatment for P. vivax parasitemia. Given the risk of hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who receive treatment with primaquine, potential recipients should be tested for G6PD deficiency. Among patients with a contraindication to primaquine therapy, treatment with chloroquine alone carries a 20% risk of relapse; extended chloroquine prophylaxis can be offered to patients who have frequent relapses.

Thursday, October 23, 2014

Community Acquired Pneumonia - Keep it simple, but not too simple.

One of the oldest (and deadliest) diseases in history, pneumonia continues being a threat. Recognizing and treating properly are the best way to minimize complications. Another good review from this week's NEJM.

What are the most common causes of CAP? Although pneumococcus remains the most commonly identified cause of CAP, the frequency with which it is implicated has declined, and it is now detected in only about 10 to 15% of inpatient cases in the United States. Other bacteria that cause CAP include Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, Pseudomonas aeruginosa, and other gram-negative bacilli. Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for CAP caused by H. influenzae and Mor. catarrhalis. P. aeruginosa and other gram-negative bacilli also cause CAP in persons who have COPD or bronchiectasis, especially in those taking glucocorticoids. There is a wide variation in the reported incidence of CAP caused by Mycoplasma pneumoniae and Chlamydophila pneumoniae (so-called atypical bacterial causes of CAP), depending in part on the diagnostic techniques that are used. During influenza outbreaks, the circulating influenza virus becomes the principal cause of CAP that is serious enough to require hospitalization, with secondary bacterial infection as a major contributor.

What evaluation do the authors recommend to determine the cause of community-acquired pneumonia in a hospitalized patient? In hospitalized patients with CAP, the authors favor obtaining Gram’s staining and culture of sputum, blood cultures, testing for legionella and pneumococcal urinary antigens, and multiplex PCR assays for Myc. pneumoniae, Chl. pneumoniae, and respiratory viruses, as well as other testing as indicated in patients with specific risk factors or exposures. A low serum procalcitonin concentration (<0.1 µg per liter) can help to support a decision to withhold or discontinue antibiotics. Results on Gram’s staining and culture of sputum are positive in more than 80% of cases of pneumococcal pneumonia when a good-quality specimen (>10 inflammatory cells per epithelial cell) can be obtained before, or within 6 to 12 hours after, the initiation of antibiotics. Blood cultures are positive in about 20 to 25% of inpatients with pneumococcal pneumonia but in fewer cases of pneumonia caused by H. influenzae or P. aeruginosa and only rarely in cases caused by Mor. catarrhalis.

What are the guidelines for treating community-acquired pneumonia in outpatients and inpatients? For outpatients without coexisting illnesses or recent use of antimicrobial agents, IDSA/ATS [Infectious Diseases Society of America and the American Thoracic Society] guidelines recommend the administration of a macrolide (provided that <25% of pneumococci in the community have high-level macrolide resistance) or doxycycline. For outpatients with coexisting illnesses or recent use of antimicrobial agents, the guidelines recommend the use of levofloxacin or moxifloxacin alone or a beta-lactam (e.g., amoxicillin–clavulanate) plus a macrolide. The authors argue, however, that a beta-lactam may be favored as empirical therapy for CAP in outpatients, since most clinicians do not know the level of pneumococcal resistance in their communities, and Str. pneumoniae is more susceptible to penicillins than to macrolides or doxycycline. Even though the prevalence of Str. pneumoniae as a cause of CAP has decreased, they raise concern about treating a patient with a macrolide or doxycycline to which 15 to 30% of strains of Str. pneumoniae are resistant. For patients with CAP who require hospitalization and in whom no cause of infection is immediately apparent, IDSA/ATS guidelines recommend empirical therapy with either a beta-lactam plus a macrolide or a quinolone alone.

What is the appropriate duration of antibiotic therapy for community-acquired pneumonia? Early in the antibiotic era, pneumonia was treated for about 5 days; the standard duration of treatment later evolved to 5 to 7 days. A meta-analysis of studies comparing treatment durations of 7 days or less with durations of 8 days or more showed no differences in outcomes, and prospective studies have shown that 5 days of therapy are as effective as 10 days and 3 days are as effective as 8. Nevertheless, practitioners have gradually increased the duration of treatment for CAP to 10 to 14 days. The authors argue that a responsible approach to balancing antibiotic stewardship with concern about insufficient antibiotic therapy would be to limit treatment to 5 to 7 days, especially in outpatients or in inpatients who have a prompt response to therapy. Pneumonia that is caused by Staph. aureus or gram-negative bacilli tends to be destructive, and concern that small abscesses may be present has led clinicians to use more prolonged therapy, depending on the presence or absence of coexisting illnesses and the response to therapy.

- Strep pneumo still is the most common bug, and is more sensitive to penicillins than macrolides or doxy.
- Uncomplicated, outpatient treatment: Macrolide or Doxy, consider adding a beta-lactam if high risk; alternatively, respiratory quinolone by it self.
- Sputum gram stain and cultures.. maybe, don't expect to get too much from them.
- 5 days of treatment is as good as 10.

Friday, October 10, 2014

Acid-Base disturbances. Physiological Approach

This has been one of those topics that give me a headache. However, having a simple approach is very helpful. This week's NEJM (Oct 9th) has an interesting review. Here are the Q&A on this topic.

What are some uses and limitations of the anion gap?
Lactic acidosis accounts for about half of the high anion gap cases, and is often due to shock or tissue hypoxia. The anion gap however, is a relatively insensitive reflection of lactic acidosis — roughly half the patients with serum lactate levels between 3.0 and 5.0 mmol per liter have an anion gap within the reference range. With a sensitivity and specificity below 80% in identifying elevated lactate levels, the anion gap cannot replace a serum lactate measurement. Nevertheless, lactate levels are not routinely drawn or always rapidly available, and a high anion gap can alert the physician that further evaluation is necessary. In addition, the anion gap should always be adjusted for the albumin concentration, because this weak acid may account for up to 75% of the anion gap. Without correction for hypoalbuminemia, the anion gap can fail to detect the presence of a clinically significant increase in anions (>5 mmol per liter) in more than 50% of cases. For every 1 g per deciliter decrement in serum albumin concentration, the calculated anion gap should be raised by approximately 2.3 to 2.5 mmol per liter.
What are the characteristics of a normal anion-gap (hyperchloremic) acidosis?
Chloride plays a central role in intracellular and extracellular acid–base regulation. A normal anion-gap acidosis will be found when the decrease in bicarbonate ions corresponds with an increase in chloride ions to retain electroneutrality, also called a hyperchloremic metabolic acidosis. This type of acidosis occurs from gastrointestinal loss of bicarbonate (e.g., because of diarrhea or ureteral diversion), from renal loss of bicarbonate that may occur in defective urinary acidification by the renal tubules (renal tubular acidosis), or in early renal failure when acid excretion is impaired. Hospital-acquired hyperchloremic acidosis is usually caused by the infusion of large volumes of normal saline (0.9%). Hyperchloremic acidosis should lead to increased renal excretion of ammonium, and measurement of urinary ammonium can therefore be used to differentiate between renal and extrarenal causes of normal anion-gap acidosis. However, since urinary ammonium is seldom measured, the urinary anion gap and urinary osmolal gap are often used as surrogate measures of excretion of urinary ammonium. The urine anion gap ([Na+] + [K+] – Cl]) is usually negative in normal anion-gap acidosis, but it will become positive when excretion of urinary ammonium (NH4+) (as ammonium chloride [NH4Cl]) is impaired, as in renal failure, distal renal tubular acidosis, or hypoaldosteronism.
What is a useful approach to the analysis and treatment of a metabolic alkalosis?
The normal kidney is highly efficient at excreting large amounts of bicarbonate, and accordingly, the generation of metabolic alkalosis requires both an increase in alkali and impairment in renal excretion of bicarbonate. Gastric fluid loss and diuretic use account for the majority of metabolic alkalosis cases. By measuring chloride in urine, one can distinguish between chloride-responsive and chloride-resistant metabolic alkalosis. If the kidneys perceive a reduced “effective circulating volume,” they avidly reabsorb filtered sodium, bicarbonate, and chloride, largely through activation of the renin–angiotensin–aldosterone system, thus reducing the concentration of urinary chloride. A (spot sample) urinary chloride concentration of less than 25 mmol per liter is reflective of chloride-responsive metabolic alkalosis. Administration of fluids with sodium chloride (usually with potassium chloride) restores effective arterial volume, replenishes potassium ions, or both with correction of metabolic alkalosis. Metabolic alkalosis with a urinary chloride concentration of more than 40 mmol per liter is mainly caused by inappropriate renal excretion of sodium chloride, often reflecting mineralocorticoid excess or severe hypokalemia (potassium concentration <2 mmol per liter). The administration of sodium chloride does not correct this type of metabolic alkalosis, which, for that reason, is called “chloride-resistant.” Diuretic-induced metabolic alkalosis is an exception because the concentration of chloride in urine may increase initially, until the diuretic effect wanes, after which the concentration of chloride in the urine will fall below 25 mmol per liter.
How is the “delta anion gap” helpful in the evaluation of mixed metabolic acid–base disorders?

In high anion-gap metabolic acidosis, the magnitude of the anion gap increase (delta AG, or ΔAG) is related to the decrease in the bicarbonate ions (Δ[HCO3]). To diagnose a high anion-gap acidosis with concomitant metabolic alkalosis or normal anion-gap acidosis, the so-called delta-delta (Δ-Δ) may be used. The delta gap is the comparison between the increase (delta) in the anion gap above the upper reference value (e.g., 12 mmol per liter) and the change (delta) in the concentration of bicarbonate ions from the lower reference value of bicarbonate ions (e.g., 24 mmol per liter). In ketoacidosis, there is a 1:1 correlation between the rise in anion-gap and the fall in concentration of bicarbonate. In lactic acidosis, the decrease in concentration of bicarbonate is 0.6 times the increase in anion gap (e.g., if the anion gap raises 10 mmol per liter, the concentration of bicarbonate should decrease about 6.0 mmol per liter). This difference is probably due to the lower renal clearance of lactate compared with keto-anions. Hydrogen buffering in cells and bone takes time to reach completion. Accordingly, the ratio may be close to 1:1 with “very acute” lactic acidosis (as with seizures or exercise to exhaustion). If the ΔAG – Δ[HCO3] in ketoacidosis or if 0.6 ΔAG – Δ[HCO3] in lactic acidosis = 0±5 mmol per liter, simple anion-gap metabolic acidosis is present. A difference greater than 5 mmol per liter suggests a concomitant metabolic alkalosis, and if the difference is less than –5 mmol per liter, a concomitant normal anion-gap metabolic acidosis is diagnosed.

Thursday, September 25, 2014

2014 AMA/ACC guidelines for the NSTE-ACS

This is a super short summary of the guidelines published on-line a couple of days ago. It basically contains what we need to know in the ED to treat these patients. There are dozens of pages on what to do after the patient leaves the department. If you are interested in that, go ahead and download the free PDF and get cozy with it. Here is the link:

You will notice that the guidelines are very similar to prior the prior edition. There are only few changes with regards with anti platelet agent choices, the elimination of CK-MB as diagnostic test, oxygen is only for those with hypoxia and a more liberal approach to coronary imaging and interventions.

OK.. now to the super condensed summary.

Class I
1. ECG within 10 mins or arrival.
2. Repeat ECG q 15-20 mins in patient who remain symptomatic and initial EKG was non-diagnostic.
3. Serial cardiac troponin I or T levels at presentation and 3 to 6 hours after symptom onset
4. Additional troponin levels should be obtained beyond 6 hours after symptom onset in patients with normal troponin levels on serial examination when changes on ECG and/or clinical presentation confer an intermediate or high index of suspicion for ACS
5. Risk scores (like GRACE score) should be used to assess prognosis in patients with NSTE-ACS
Class IIa
1. Risk-stratification models can be useful in management (like TIMI).
2. Get ECG leads V7 to V9 in patients whose 
initial ECG is nondiagnostic and who are at intermediate/high risk of ACS looking for posterior MI.
Class IIb
1. Continuous monitoring with 12-lead ECG
2. Measurement of B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide may be considered to assess risk in patients with suspected ACS

Biomarkers: Diagnosis
Class I
1. If the time of symptom onset is ambiguous, the time of presentation should be considered the time of onset for assessing troponin values
Class III: No Benefit

1. If you have troponins in your lab, forget about creatine kinase myocardial isoenzyme (CK-MB) and myoglobin are not useful for diagnosis of ACS

Biomarkers: Prognosis
Class I

1. The presence and magnitude of troponin elevations are useful for short- and long-term prognosis

Discharge from the ED
Class IIa
1. OK to admit at risk patients to chest pain units for repeat ECG's an trops at 3- to 6-hour intervals
2. Patients with normal serial ECGs and cardiac troponins can have a treadmill ECG, stress myocardial perfusion imaging, or stress echocardiography before discharge or within 72 hours after discharge.
3. Reasonable alternatives are coronary computed tomography angiography to assess coronary artery anatomy or rest myocardial perfusion imaging with a technetium-99m radiopharmaceutical to exclude myocardial ischemia.
4. Those who go home, get daily aspirin, short-acting nitroglycerin, and other medication if appropriate (e.g., beta blockers), with instructions about activity level and clinician follow-up.

Early Hospital Care
Class I

1. Supplemental oxygen should be administered to patients with NSTE-ACS with arterial oxygen saturation less than 90%, respiratory distress, or other high-risk features of hypoxemia.
Class I
1. Patients with NSTE-ACS with continuing ischemic pain should receive sublingual nitroglycerin 
(0.3 mg–0.4 mg) every 5 minutes for up to 3 doses, after which an assessment should be made about the need for intravenous nitroglycerin if not contraindicated
2. Intravenous nitroglycerin is indicated for patients with NSTE-ACS for the treatment of persistent ischemia, heart failure (HF), or hypertension.
Analgesic Therapy
Class IIb

1. If no contrainfications, Morphine for non-controlled ischemic pain is just fine.
Class III:

1. Don’t use NSAID’s and if they are taking NSAID’s for other reasons, stop it.
Beta-Adrenergic Blockers
Class I
1. Oral beta-blocker therapy should be initiated within the first 24 hours in patients who do not have any of the following: 1) signs of HF, 2) evidence of low-output state, 3) increased risk for cardiogenic shock, or 4) other contraindications to beta blockade (e.g., PR interval >0.24 second, second- or third-degree heart block without a cardiac pacemaker, active asthma, or reactive airway disease)
2. In patients with concomitant NSTE-ACS, stabilized HF, and reduced systolic function, it is recommended to continue beta-blocker therapy with 1 of the 3 drugs proven to reduce mortality in patients with HF: sustained-release metoprolol succinate, carvedilol, or bisoprolol.
3. Patients with documented contraindications to beta blockers in the first 24 hours of NSTE-ACS should be reevaluated to determine their subsequent eligibility. 

1. It is reasonable to continue beta-blocker therapy in patients with normal left ventricular (LV) function with NSTE-ACS 
III: Harm
1. Administration of intravenous beta blockers is potentially harmful in patients with NSTE-ACS who have risk factors for shock (poor EF, tachycardic, know myocardiopathy)
Calcium Channel Blockers
Class I
1. In patients with NSTE-ACS, continuing or frequently recurring ischemia, and a contraindication to beta blockers, a nondihydropyridine calcium channel blocker (CCB) (e.g., verapamil or diltiazem) should be given as initial therapy in the absence of clinically significant LV dysfunction, increased risk for cardiogenic shock, PR interval greater than 0.24 second, or second- or third- degree atrioventricular block without a cardiac pacemaker
2. CCBs are recommended for ischemic symptoms when beta blockers are not successful, are contraindicated, or cause unacceptable side effects. 
Class III: Harm

1. Immediate-release nifedipine should not be administered to patients with NSTE-ACS in the absence of beta-blocker therapy
Antiplatelet Agents
Class I
1. If non-allergic, give Aspirin to everyone (162 mg to 325 mg) as soon as possible after presentation, and a maintenance dose of aspirin (81 mg/d to 162 mg/d) should be continued indefinitely
2. If Aspirin allergic, give clopidogrel followed by a daily maintenance dose should be administered
Class IIa

1. It is reasonable to use ticagrelor in preference to clopidogrel in patients with NSTE ACS who undergo an early invasive or ischemia-guided strategy.
Class IIb

1. In patients with NSTE-ACS treated with an early invasive strategy and dual anti platelet therap  (DAPT) with intermediate/high-risk features (e.g., positive troponin), a glycoprotein (GP) IIb/IIIa inhibitor may be considered as part of initial antiplatelet therapy. Preferred options are eptifibatide or tirofiban.


Class I
1. In patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended for all patients irrespective of initial treatment strategy. Treatment options include:
- Enoxaparin: 1 mg/kg subcutaneous (SC) every 12 hours (reduce dose to 1 mg/kg SC once daily in patients with creatinine clearance [CrCl] <30 mL/min), continued for the duration of hospitalization or until percutaneous coronary intervention (PCI) is performed. An initial intravenous loading dose is 30 mg

- Bivalirudin: 0.10 mg/kg loading dose followed by 0.25 mg/kg per hour (only in patients managed with an early invasive strategy), continued until diagnostic angiography or PCI, with only provisional use of GP IIb/IIIa inhibitor, provided the patient is also treated with DAPT

- Fondaparinux: 2.5 mg SC daily, continued for the duration of hospitalization or until PCI is performed

- If PCI is performed while the patient is on fondaparinux, an additional anticoagulant with anti-IIa activity (either UFH or bivalirudin) should be administered because of the risk of catheter thrombosis

- UFH IV: initial loading dose of 60 IU/kg (maximum 4,000 IU) with initial infusion of 12 IU/kg per hour (maximum 1,000 IU/h) adjusted per activated partial thromboplastin time to maintain therapeutic anticoagulation according to the specific hospital protocol, continued for 48 hours or until PCI is performed

Class III: Harm

1. In patients with NSTE-ACS (i.e., without ST elevation, true posterior MI, or left bundle-branch block not known to be old), intravenous fibrinolytic therapy should not be used.
Ischemia-Guided Strategy Versus Early Invasive Strategies

Early Invasive and Ischemia-Guided Strategies
Class I
1. An urgent/immediate invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures).
2. An early invasive strategy (diagnostic angiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in initially stabilized patients with NSTE- ACS (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events
Class IIa

1. It is reasonable to choose an early invasive strategy (within 24 hours of admission) over a delayed invasive strategy (within 24 to 72 hours) for initially stabilized high-risk patients with NSTE-ACS. For those not at high/intermediate risk, a delayed invasive approach is reasonable

1. In initially stabilized patients, an ischemia-guided strategy may be considered for patients with NSTE ACS (without serious comorbidities or contraindications to this approach) who have an elevated risk for clinical events  
2. The decision to implement an ischemia-guided strategy in initially stabilized patients (without serious comorbidities or contraindications to this approach) may be reasonable after considering clinician and patient preference.
III: No Benefit

1. An early invasive strategy (i.e., diagnostic angiography with intent to perform revascularization) is not recommended in patients with:
- Extensive comorbidities (e.g., hepatic, renal, pulmonary failure, cancer), in whom the risks of revascularization and comorbid conditions are likely to outweigh the benefits of revascularization.  
- Acute chest pain and a low likelihood of ACS who are troponin- negative, especially women.

Ufff. That was painful !  But not as painful as the 71 pages of the whole document. Now go and tell your friends that NSTE-ACS has new guidelines with just a few changes.

Thursday, July 31, 2014

Scorpion Envenomation. Not so bad, but when it bad... is BAD!

Still is summer time and in some parts of the world, scorpions are a threat. There are dozens of varieties to chose from. Here are some basics about the patophysiology of Scorpion Envenomation. From this week's NEJM.

What are the general characteristics of scorpion stings?
Most scorpion stings cause localized pain, whereas only an estimated 10% of stings, even from the most dangerous scorpions, result in severe systemic envenomation. Edema, erythema, paresthesias, muscle fasciculations, and numbness may occur at the site of the sting. It is often difficult to see the sting site or to identify inflammation at the site, despite substantial local pain. Most cases of severe envenomation occur in children. Systemic envenomation is characterized by neuromuscular abnormalities resulting from effects on the somatic and cranial nerves, both cholinergic and adrenergic excitation of the autonomic nervous system, pulmonary edema, and cardiac effects.
What are the autonomic effects of scorpion stings?
Excitation of the autonomic nervous system is characterized by both parasympathetic and sympathetic responses. Parasympathetic, cholinergic effects may include hypersalivation, profuse diaphoresis, lacrimation, miosis, diarrhea, vomiting, bradycardia, hypotension, increased respiratory secretions, and priapism. Sympathetic, adrenergic effects include tachycardia, hypertension, mydriasis, hyperthermia, hyperglycemia, agitation, and restlessness. Whereas most parasympathetic effects tend to occur early, sympathetic effects persist because of the release of catecholamines and are responsible for severe envenomation.
What are possible cardiovascular complications of scorpion envenomation? A range of cardiac conduction abnormalities occur in about one third to one half of patients with systemic envenomation. These effects include atrial tachycardia, ventricular extrasystoles, T-wave inversion, ST-T wave changes, and, less frequently, bundle-branch block. Increased autonomic stimulation caused by increased vagal effects on the heart and sympathetic stimulation are the probable causes of these effects. Hypertension is common and occurs early in response to sympathetic stimulation. Hypotension is less common, occurs with the development of severe envenomation, and often requires intervention with vasopressors and fluid resuscitation. Many factors are at play in the development of hypotension, with cholinergic stimulation causing vasodilation, fluid loss, and myocardial depression. Cardiac dysfunction resulting from catecholamine-induced myocarditis and myocardial ischemia complicates severe envenomation from androctonus, buthus, mesobuthus, and tityus scorpions. This complication may result in pulmonary edema and cardiogenic shock.

What are the principles of treatment for cases of severe scorpion envenomation? The specific treatment is the administration of antivenom combined with symptomatic and supportive treatment, including prazosin and dobutamine in patients with cardiovascular toxic effects and benzodiazepines when there is neuromuscular involvement. Symptoms related to the site of the sting should be managed with appropriate analgesia with acetaminophen and antiinflammatory agents, depending on severity. Once severe envenomation has developed, the administration of antivenom may be less effective, since its primary therapeutic action is to bind toxins; it does not reverse established pathophysiological injury, such as excess levels of catecholamine, pulmonary edema, and cardiogenic shock.
- Scorpion envenomation are rarely fatal, but children are at high risk.
- For most, supportive treatment is fine if no signs of nervous or cardiac system involvement. 
- If is going to be bad, it goes from bad to worse very quickly. Therefore, if antivenom is available, give it early and transfer sooner rather than later.
- Prazosin, an alfa blocker, and dobutamine in combination for patients with cardiovascular symptoms. And benzos for neuromuscular involvement.
- Not all scorpions are scary, some can also be cute... like this one!