Severe Cardiovascular Collapse Research Articles

Anaesthetic management of posterior mediastinal mass: a case report

Posterior mediastinal mass surgery is a challenge to the anaesthetist in terms of airway obstruction, compression of great vessels due to mass effect of tumour and severe cardiovascular and/or respiratory collapse. This may occur following decrease in chest wall tone associated with neuromuscular blockade. In this case study, we report an 8-year-old male child presented with a large posterior mediastinal mass, displacing and partially encasing the aorta at our institution, SMS Medical College & Hospitals, Jaipur, Rajasthan. Mass was removed by left thoracotomy; endotracheal tube was advanced into the right bronchus to ventilate the right lung to improve access in the surgical field because tumour was situated on the left side. While dissecting the mass, there was considerable blood loss. This was replaced with hydroxyethyl starch and whole blood. Patient was extubated next day with uneventful recovery.

Optimal management of acute nonrenal adverse reactions to iodine-based contrast media

Acute adverse reactions to iodine-based contrast media occur within 60 minutes of administration. The reactions range from mild (flushing, arm pain, nausea/vomiting, headache) to moderate (bronchospasm, hypotension), and severe (cardiovascular collapse, laryngeal edema, convulsions, arrhythmias). Most acute adverse reactions occur in an unpredictable manner. Use of the older group of ionic iodine-based contrast agents increases the risk of acute adverse reactions. Other risk factors include previous reactions to contrast media, asthma, and allergic conditions. The exact pathophysiology of the acute adverse reactions is unknown, but some of the reactions are pseudoallergic mimicking type 1 allergic reactions. As antibodies against contrast media have not been consistently demonstrated, the reactions are, in most cases, not truly allergic in nature. Most of the severe and fatal adverse reactions occur within the first 20 minutes after injection. Thus, it is important that patients are observed in the radiology department during this period. The radiologist should be near the room where contrast media is administered, and be ready to treat any acute nonrenal adverse reaction. Appropriate drugs and resuscitation equipment should be in/near the room where the contrast media is administered. The important first-line management of acute adverse reactions includes the establishment of an adequate airway, oxygen supplementation by mask, intravenous fluid administration, and measurement of blood pressure and heart rate. When severe anaphylactoid reactions occur, adrenaline should be given intramuscularly. Only one concentration of adrenaline (1:1000-1 mg/mL) should be available in the radiology department to avoid dosing errors in stressful acute settings. Resuscitation team specialists should be the only ones giving intravenous adrenaline. It is important that all radiologists maintain the capability of performing first-line treatment of acute adverse reactions

Sudden syncopal attack after postobstructed diuresis under combined spinal epidural anesthesia

Micturition is clinically well-known as a factor that may cause hypotension, bradycardia, and if severe, syncope. However, the mechanism of syncope during micturition is not completely understood. Vasodilatation, bradycardia, and reflex car diovascular depression are all called by various terms including vasovagal syncope, Bazold-Jarisch reflex, and neurocardiogenic syncope [1]. The neurally-mediated syncope includes true and situational syncope that can take place in various situations such as blood loss, cough, sneeze, micturition and lifting up a heavy load. A case of a 71 year-old man under combined spinal epidural anesthesia for total knee replacement, in which the operation were performed without knowing that a Foley catheter installed had been obstructed, and severe bradycardia, hypotension, and loss of consciousness occurred immediately after moving the pa tient to the recovery room following micturition were described. The patient had a history of syncope. Preoperative cardiac test was normal. At the operation room, heart rate and blood pressure were 70 /min and 170/90 mmHg. Beginning with the sufficient administration of fluid, the regional anesthesia was performed and the sensory block was verified up to the T4 der matome. A forced air warmer was used to maintain the body temperature. At the end of operation, 8 ml of 0.15% levobupivacaine was injected through the epidural catheter, and then a mixture of anesthetics was continuously injected. Intraoperative systolic blood pressure were ranged from 110 to 190 mmHg, diastolic pressure 65 to 105 mmHg, heart rate 52 to 70 /min, and estimated blood loss was approximately 500 ml. Although the total amount of fluid was approximately 1,000 ml, no urine out put was observed. Just before leaving the operation room, it was found that the tip of the Foley catheter was obstructed. When the catheter was opened, about 700 ml of urine was discharged. At that time, the vital signs were normal and consciousness clear. Finding that the sensory block level had come down to the T12 dermatome, the patient was moved to the recovery room. Immediately after arriving at the recovery room, the heart rate was drastically reduced from 70 /min to 30 /min or below, the blood pressure was 50/30 mmHg, and consciousness was lost. Promptly, 0.5 mg of atropine sulfate and 10 mg of ephedrine were administered, and the patient-controlled epidural anal gesia (PCEA) was stopped. Following the treatment, the heart rate recovered to 60 /min and the blood pressure to 110/80 mmHg, and subsequently, the consciousness of the patient was recovered. While the patient remained in the recovery room, no abnormal findings were observed. Micturition syncope was con firmed that head-tilt test done after the operation was positive. The main causes of consciousness loss when awakening from anesthesia include metabolic anomalies such as hypoglycemia, hyponatremia, hypoxia and severe cardiovascular collapse. However, based on the fact that the patient had no findings of cardiac abnormalities, the patient in this case might have experienced reflex micturition syncope. Micturition syncope is one type of situational syncope that occurs due to neural mediation, and usually occurs in healthy men after alcohol hyperingestion [2]. Sumiyoshi et al. [2] mentioned sleeping under warm blankets and administration of a vasodilator can be factors that cause a reduction in the peripheral arterial blood resistance in the lower extremities and reported that the Valsalva maneuver is a factor

Obesity supine death syndrome revisited

To the Editors: Given the current worldwide epidemic of obesity, it is likely that an increasing number of obese patients will be admitted to hospital in the future [1]. Caring for morbidly obese patients is a critical task that is time-consuming, and requires a trained and motivated staff. One particular hurdle to overcome in the management of these patients is positioning. Unfortunately, this is rarely considered a high priority issue in the emergency setting, despite the potential for dramatic cardiopulmonary complications resulting from the supine positioning of massively obese patients. In extreme cases, it may even result in death. This catastrophic phenomenon has been called the “obesity supine death syndrome”. However, only two other cases of this condition have been previously reported [2], and therefore it remains relatively unfamiliar to most physicians. We recently managed a 44-yr-old male with a body mass index of 80 kg·m−2 who immediately developed severe hypoxaemia, seizures and cardiovascular collapse when placed in the supine position. This case gives us an insight into understanding the underlying mechanisms leading to position-induced cardiorespiratory decompensation in morbidly obese patients. The patient …

Intravenous injection of autologous amniotic fluid induces transient thrombocytopenia in a gravid rabbit model of amniotic fluid embolism

Amniotic fluid embolism (AFE) is a rare but catastrophic complication of pregnancy characterized by severe hypotension, cardiovascular collapse, and massive consumptive coagulopathy. Several animal models of this syndrome have been proposed, but most have yielded inconclusive results. The objective of this study was to develop a suitable animal model of AFE. Twelve rabbits in late gestation (25 days) were used. Amniotic fluid was collected from the fetal amniotic sacs after laparotomy, and autologous fluid was injected into 6 rabbits via the left auricular vein. Six other rabbits received saline (control group). Blood pressure, platelet counts, and coagulation variables were measured at baseline and at various intervals for 60 minutes after injection. The in vitro effect of amniotic fluid on coagulation was assessed by thrombelastographic (TEG) analysis. Injection of amniotic fluid did not reproduce clinical signs of AFE and had no effect on activated partial thromboplastin time (aPTT), prothrombin time (PT), or Factor VIII activity. However, significant thrombocytopenia was observed 5 minutes after administration of amniotic fluid and resolved by 60 minutes. In vitro addition of amniotic fluid to blood resulted in accelerated clotting on TEG tracings. The syndrome of AFE was not reproduced in this rabbit model. However, injection of autologous amniotic fluid induced a transient and severe thrombocytopenia. Moreover, TEG analysis indicated that amniotic fluid could initiate the coagulation cascade. Other factors such as the presence of meconium in amniotic fluid may be needed to provoke more severe clinical signs.

Severe sodium channel blockade and cardiovascular collapse due to a massive Lamotrigine overdose

Background. Cardiac arrest due to lamotrigine (LTG) has been reported after co-ingestion with bupropion, but severe sodium channel blockade in the absence of other toxins has not been described. We report a case of cardiac arrest and status epilepticus following a massive LTG overdose. Case Report. A 48 year-old female was brought to the ED with seizure-like activity subsequent to ingesting 7.5 g of LTG. Vital signs were HR 131, BP 107/68, T 99.4°F, RR 16. She was intubated in the ED for a low GCS. Initial ECG demonstrated a narrow-complex normal sinus rhythm, and her labs were unremarkable. Three hours after intubation she developed status epilepticus, and a pulseless wide-complex tachycardia. She was aggressively resuscitated during which time pulses were periodically reestablished, but lost each time seizures recurred. She was not stabilized until the convulsions were terminated with vecuronium. Her post-resuscitation ECG demonstrated a junctional tachycardia with a 3 mm R-wave in aVR. The LTG level was 74.7 mcg/ml (therapeutic: 3–14 mcg/ml). Comprehensive LC-MS/MS drug screen was negative for all screened compounds. Discussion. This is the first report of cardiovascular collapse due to LTG with the highest drug concentration to date. Conclusion. The degree of neurologic and cardiovascular toxicity seen in this case are novel and illustrate the potential for severe sodium channel blockade after massive LTG poisonings. Drug levels are not clinically relevant in the acute setting due to the time delay in obtaining results, and recurrent seizure activity may be the only clinical finding that precedes severe cardiac toxicity.

Complications of Endotracheal Intubation in Intensive Care Unit

Aim: We aimed to compare patients who developed complications during endotracheal intubation and who did not develop any complication in the Medical Intensive Care Unit. Material and Methods: We enrolled 39 patients into the study. Patients intubated outside the intensive care unit (emergency service, prior to operation) were excluded. All intubation procedures were performed by residents in internal medicine. Data about the patient and complications were recorded by the same person. Results: At least one complication was seen in 41% of all patients. Life-threatening complications such as severe hypoxemia (12%) and severe cardiovascular collapse (7%) were found. Difficult intubation (23%), aspiration (10%), esophageal intubation (10%), dental injury (10%), and dangerous agitation (3%) were found as moderate complications. Acute respiratory failure was the most common reason for intensive care unit admission (59%) and intubation (74%). Within one hour before intubation, the highest and lowest mean heart rate was higher than those who developed complications. No complications were observed in patients who were intubed at the first attempt. All complications occurred in patients who had two or more trials. Conclusion: Complications of endotracheal intubation is an important problem in intensive care units. Intubation success on the first attempt prevents complications. As the number of endotracheal intubation with the assistance of laryngoscopy increased, it was seen that complications related to the procedure also increased. (Yogun Bakim Derg 2011; 2: 39-43)

Tracheal intubation in the ICU: Life saving or life threatening?

Tracheal intubation (TI) is a routine procedure in the intensive care unit (ICU), and is often life saving. However, life-threatening complications occur in a significant proportion of procedures, making TI perhaps one the most common but underappreciated airway emergencies in the ICU. In contrast to the controlled conditions in the operating room (OR), the unstable physiologic state of critically ill patients along with underevaluation of the airways and suboptimal response to pre-oxygenation are the major factors for the high incidence of life-threatening complications like severe hypoxaemia and cardiovascular collapse in the ICU. Studies have shown that strategies planned for TI in the OR can be adapted and extrapolated for use in the ICU. Non-invasive positive-pressure ventilation for pre-oxygenation provides adequate oxygen stores during TI for patients with precarious respiratory pathology. The intubation procedure should include not only airway management but also haemodynamic, gas exchange and neurologic care, which are often crucial in critically ill patients. Hence, there is a necessity for the implementation of an Intubation Bundle during routine airway management in the ICU. Adherence to a plan for difficult airway management incorporating the use of intubation aids and airway rescue devices and strategies is useful.

Laxatives or methylnaltrexone for the management of constipation in palliative care patients

Background: Constipation is common in palliative care; it can generate considerable suffering due to the unpleasant physical symptoms. In the first Cochrane Review on effectiveness of laxatives for the management of constipation in palliative care patients, published in 2006, no conclusions could be drawn because of the limited number of evaluations. This article describes the first update of this review. / Objectives: To determine the effectiveness of laxatives or methylnaltrexone for the management of constipation in palliative care patients. / Search methods: We searched databases including MEDLINE and CENTRAL (The Cochrane Library) in 2005 and in the update to August 2010. / Selection criteria: Randomised controlled trials (RCTs) evaluating laxatives for constipation in palliative care patients. In the update we also included RCTs on subcutaneous methylnaltrexone; an opioid-receptor antagonist that is now licensed for the treatment of opioid-induced constipation in palliative care when response to usual laxative therapy is insufficient. / Data collection and analysis: Two authors assessed trial quality and extracted data. The appropriateness of combining data from the studies depended upon clinical and outcome measure homogeneity. / Main results: We included seven studies involving 616 participants; all under-reported methodological features. In four studies the laxatives lactulose, senna, co-danthramer, misrakasneham, and magnesium hydroxide with liquid paraffin were evaluated. In three methylnaltrexone. In studies comparing the different laxatives evidence was inconclusive. Evidence on subcutaneous methylnaltrexone was clearer; in combined analysis (287 participants) methylnaltrexone, in comparison with a placebo, significantly induced laxation at 4 hours (odds ratio 6.95; 95% confidence interval 3.83 to 12.61). In combined analyses there was no difference in the proportion experiencing side effects, although participants on methylnaltrexone suffered more flatulence and dizziness. No evidence of opioid withdrawal was found. In one study severe adverse events, commonly abdominal pain, were reported that were possibly related to methylnaltrexone. A serious adverse event considered to be related to the methylnaltrexone also occurred; this involved a participant having severe diarrhoea, subsequent dehydration and cardiovascular collapse. / Authors' conclusions: The 2010 update found evidence on laxatives for management of constipation remains limited due to insufficient RCTs. However, the conclusions of this update have changed since the original review publication in that it now includes evidence on methylnaltrexone. Here it found that subcutaneous methylnaltrexone is effective in inducing laxation in palliative care patients with opioid-induced constipation and where conventional laxatives have failed. However, the safety of this product is not fully evaluated. Large, rigorous, independent trials are needed.

Genetic deletion of NOS3 increases lethal cardiac dysfunction following mouse cardiac arrest

Study aimsCardiac arrest mortality is significantly affected by failure to obtain return of spontaneous circulation (ROSC) despite cardiopulmonary resuscitation (CPR). Severe myocardial dysfunction and cardiovascular collapse further affects mortality within hours of initial ROSC. Recent work suggests that enhancement of nitric oxide (NO) signaling within minutes of CPR can improve myocardial function and survival. We studied the role of NO signaling on cardiovascular outcomes following cardiac arrest and resuscitation using endothelial NO synthase knockout (NOS3−/−) mice. MethodsAdult female wild-type (WT) and NOS3−/− mice were anesthetized, intubated, and instrumented with left-ventricular pressure-volume catheters. Cardiac arrest was induced with intravenous potassium chloride. CPR was performed after 8min of untreated arrest. ROSC rate, cardiac function, whole-blood nitrosylhemoglobin (HbNO) concentrations, heart NOS3 content and phosphorylation (p-NOS3), cyclic guanosine monophosphate (cGMP), and phospho-troponin I (p-TnI) were measured. ResultsDespite equal quality CPR, NOS3−/− mice displayed lower rates of ROSC compared to WT (47.6% [10/21] vs. 82.4% [14/17], p<0.005). Among ROSC animals, NOS3−/− vs. WT mice exhibited increased left-ventricular dysfunction and 120min mortality. Prior to ROSC, myocardial effectors of NO signaling including cGMP and p-TnI were decreased in NOS3−/− vs. WT mice (p<0.05). Following ROSC in WT mice, significant NOS3-dependent increases in circulating HbNO were seen by 120min. Significant increases in cardiac p-NOS3 occurred between end-arrest and 15min post-ROSC, while total NOS3 content was increased by 120min post-ROSC (p<0.05). ConclusionsGenetic deletion of NOS3 decreases ROSC rate and worsens post-ROSC left-ventricular function. Poor cardiovascular outcomes are associated with differences in NOS3-dependent myocardial cGMP signaling and circulating NO metabolites.

Severe pulmonary hypertension associated with the acute motor sensory axonal neuropathy subtype of Guillain-Barré syndrome

To evaluate pulmonary hypertension associated with acute motor sensory axonal neuropathy subtype of Guillain-Barré syndrome. Guillain-Barré syndrome consists of a group of autoimmune disorders that generally manifest as symmetric, progressive, ascending paralysis. There are five subtypes of Guillain-Barré syndrome, and autonomic involvement has been described in all subtypes, including cardiovascular, vasomotor, or pseudomotor dysfunction of both the sympathetic and parasympathetic systems. Case report. Tertiary care pediatric intensive care unit. Three-yr-old female patient. None. Serial measurements of pulmonary artery pressure. We report the case of a young girl with acute motor sensory axonal neuropathy who presented with severe cardiovascular collapse secondary to severe pulmonary hypertension. In this patient, multiple factors may have played a role in the development of pulmonary hypertension including autonomic dysfunction, hypoventilation, and immobility as a risk for thrombosis and pulmonary emboli. It is possible that many other individuals suffering from severe forms of Guillain-Barré syndrome, especially those with significant autonomic dysfunction, may actually have undiagnosed and therefore untreated pulmonary hypertension. Therefore, it is recommended that clinicians caring for critically ill children with Guillain-Barré syndrome have a high index of suspicion for pulmonary hypertension and consider echocardiography if there are clinical signs of this potentially fatal process.

An intervention to decrease complications related to endotracheal intubation in the intensive care unit: a prospective, multiple-center study

To determined whether the implementation of an intubation management protocol leads to the reduction of intubation-related complications in the intensive care unit (ICU). Two-phase, prospective, multicenter controlled study. Three medical-surgical ICUs in two university hospitals. Two hundred three consecutive ICU patients required 244 intubations. All intubations performed during two consecutive phases (a 6-month quality control phase followed by a 6-month intervention phase based on the implementation of an ICU intubation bundle management protocol) were evaluated. The ten bundle components were: preoxygenation with noninvasive positive pressure ventilation, presence of two operators, rapid sequence induction, cricoid pressure, capnography, protective ventilation, fluid loading, preparation and early administration of sedation and vasopressor use if needed. The primary end points were the incidence of life-threatening complications occurring within 60 min after intubation (cardiac arrest or death, severe cardiovascular collapse and hypoxemia). Other complications (mild to moderate) were also evaluated. Baseline characteristics, including demographic data and reason for intubation (mainly acute respiratory failure), were similar in the two phases. The intubation procedure in the intervention phase (n = 121) was associated with significant decreases in both life-threatening complications (21 vs. 34%, p = 0.03) and other complications (9 vs. 21%, p = 0.01) compared to the control phase (n = 123). The implementation of an intubation management protocol can reduce immediate severe life-threatening complications associated with intubation of ICU patients.

Fatal Venous Air Embolism Following Intravenous Infusion*

Venous air embolism has been reported as a complication of invasive diagnostic and therapeutic procedures or accidental trauma. Little is known about the incidence of air embolism after minimal intravenous manipulations such as the insertion of a peripheral intravenous cannula. Only when large amounts of air sufficient enough to block the cardiovascular system enter, the patient develops symptoms and signs of severe neurological injury, cardiovascular collapse, or death. The dead body of a 14-year-old boy was brought for postmortem examination with allegations of death from negligence during treatment. He was treated for pain in the abdomen in a hospital by attendants in telephonic consultation with a medical practitioner. Following intravenous infusions, the boy died suddenly in respiratory distress. Gross findings indicated the death to be from venous air embolism. Chemical analysis, histopathology, and microbiology ruled out other causes of death. Dilemmas of the case with difficulties in diagnosis are being presented herewith.

Management of the patient with a large anterior mediastinal mass: recurring myths

This editorial review summarizes the current anesthetic management of patients with anterior mediastinal masses. With increased appreciation of the correct intraoperative management of these cases severe intraoperative respiratory or cardiovascular collapse is less likely to occur during general anesthesia. Maintenance of spontaneous ventilation is the anesthetic goal whenever possible. Major life-threatening complications now occur more frequently postoperatively. General anesthesia is not safe in patients with severe positional symptoms from an anterior mediastinal mass. With modern imaging techniques, general anesthesia is rarely needed for diagnostic procedures in these patients. Preoperative flow-volume loops are not useful in the management of these patients and the concept of cardiopulmonary bypass on 'standby' is not appropriate during induction of anesthesia.

Insulin effects on myocardial function and bioenergetics in l-bupivacaine toxicity in the isolated rat heart

A positive effect of insulin-glucose-potassium infusion in severe bupivacaine-induced cardiovascular collapse has been described in vivo. It has been speculated that an antagonistic influence of insulin on sodium channel inhibition, transient outward potassium current, calcium-dependent adenosine triphosphatase or even improved myocardial energetics may be responsible for this effect. Using an isolated heart model, we therefore sought to further elucidate insulin effects in l-bupivacaine-induced myocardial depression. An isolated rat heart constant-pressure perfused, non-recirculating Langendorff preparation was used. Hearts were exposed to l-bupivacaine 5 microg mL(-1) and insulin 10 mIU mL(-1). Heart rate, systolic pressure, the first derivative of left ventricular pressure (+dP/dt), coronary flow, double product, PR and QRS intervals were recorded. Hearts were freeze-clamped and high-performance liquid chromatography measurement of the total adenine nucleotide pool was performed. l-Bupivacaine led to a significant decrease in heart rate, +dP/dt, systolic pressure, coronary flow and double product, and to an increase in PR and QRS. Insulin exerted a positive inotropic effect, significantly augmenting +dP/dt and systolic pressure in both l-bupivacaine-treated and control hearts. Heart rate, coronary flow, total adenine nucleotides, PR and QRS were not significantly changed by the insulin intervention. Insulin did not have a significant effect on total adenine nucleotides in controls and in l-bupivacaine-treated hearts. However, it does exert a positive inotropic action in bupivacaine-induced myocardial depression. We conclude that the positive effect of insulin application lies in positive inotropic action and not in changes in total adenine nucleotides.

From the Laboratory to the Bedside

From the Laboratory to the Bedside

First report of supraventricular tachycardia after intravenous pulse methylprednisolone therapy, with a brief review of the literature

The occurrence of supraventricular tachycardia after high-dose intravenous methylprednisolone pulse therapy (HIVMPT) in a patient with active rheumatoid arthritis is described for the first time. This case report further expands the range of arrhythmias that can occur with HIVMPT. Other arrhythmias previously reported to occur after HIVMPT include atrial fibrillation, atrial flutter, junctional rhythm, and ventricular tachycardia. To the best of our knowledge, supraventricular tachycardia has not been reported previously, although severe bradycardia, hypotension, asystole, cardiovascular collapse, and sudden death have been documented. A review of the literature indicates that these case reports not withstanding, HIVMPT is generally safe, and cardiovascular toxicity is rare. However, close supervision with repeated measurements of blood pressure, electrocardiogram, and blood electrolytes is mandatory during and immediately after HIVMPT, especially for patients with pre-existing cardiovascular disease, and the lowest effective dose of methylprednisolone should be infused at a slow rate.

Pulseless electrical activity after induction of anesthesia: A witnessed cardiac rupture

Acute ventricularrupture leads to a sudden accumulation of blood in the pericar-dial space, resulting in reduced diastolic filling of the ventriclesand decreased cardiac output. Patients may present with symp-toms of cardiogenic shock or severe cardiovascular collapse. Ina chronic/subacute rupture, the clinical presentations are eithernonspecific or masked by the symptoms of a coexisting MI andcongestive heart failure. The present report is a case of cata-strophic cardiovascular collapse during induction of anesthesiain a patient who had a subacute post-MI left ventricular freewall rupture.

The use of a continuous infusion of epinephrine for anaphylactic shock during labor

Background Anaphylaxis is a potentially life threatening, acute, and severe systemic reaction that occurs after the reexposure to a specific antigen. This immunoglobulin E-mediated process is the result of the action of basophils and mast cell mediators, causing severe brochospasm, laringospasm, angioedema, urticaria, and cardiovascular collapse. Case We present a case of anaphylactic shock during labor secondary to administration of ampicillin for group B streptococcus prophylaxis. Generalized itching and hives were soon followed by severe maternal hypotension and tachycardia and prolonged fetal bradycardia. These symptoms responded partially to the administration of fluids and parenteral epinephrine. A continuous infusion of epinephrine was required for persistent maternal symptoms. The infusion did not result in further fetal compromise. The patient delivered a healthy fetus 4 hours after the start of the epinephrine infusion. Conclusion This case supports the use of parenteral (intravenous) epinephrine for the treatment of anaphylactic reactions during pregnancy.

Microbiological, Biological, and Chemical Weapons of Warfare and Terrorism

Microbiological, biological, and chemical toxins have been employed in warfare and in terrorist attacks. In this era, it is imperative that health care providers are familiar with illnesses caused by these agents. Botulinum toxin produces a descending flaccid paralysis. Staphylococcal enterotoxin B produces a syndrome of fever, nausea, and diarrhea and may produce a pulmonary syndrome if aerosolized. Clostridium perfringens epsilon-toxin could possibly be aerosolized to produce acute pulmonary edema. Ricin intoxication can manifest as gastrointestinal hemorrhage after ingestion, severe muscle necrosis after intramuscular injection, and acute pulmonary disease after inhalation. Nerve agents inhibit acetylcholinesterase and thus produce symptoms of increased cholinergic activity. Ammonia, chlorine, vinyl chloride, phosgene, sulfur dioxide, and nitrogen dioxide, tear gas, and zinc chloride primarily injure the upper respiratory tract and the lungs. Sulfur mustard (and nitrogen mustard) are vesicant and alkylating agents. Cyanide poisoning ranges from sudden-onset headache and drowsiness to severe hypoxemia, cardiovascular collapse, and death. Health care providers should be familiar with the medical consequences of toxin exposure, and understand the pathophysiology and management of resulting illness.