Educational Forum/Thread Game

[itku2er]

Hypertensive Urgency, Emergency, Crisis, and Treatment

Traditionally, hypertensive crises have been divided into emergencies and urgencies. Hypertensive emergencies are severe elevations in blood pressure (BP) that are complicated by evidence of progressive target organ dysfunction, and will require immediate BP reduction (not necessarily to normal ranges) to prevent or limit target organ damage. Examples include: hypertensive encephalopathy, intracranial hemorrhage, unstable angina pectoris, or acute myocardial infarction, acute left ventricular failure with pulmonary edema, dissecting aneurysm, or eclampsia. While the level of BP at the time of presentation is usually very high (greater than 180/120 mm Hg), keep in mind that it is not the degree of BP elevation, but rather the clinical status of the patient that defines a hypertensive emergency. For example, a BP of 160/100 mm Hg in a 60-year-old patient who presents with acute pulmonary edema represents a true hypertensive emergency.

Hypertensive urgencies are severe elevations of BP but without evidence of progressive target organ dysfunction and would be better defined as severe elevations in BP without acute, progressive target organ damage. A traditional term “urgency” has led to aggressive and often excessive treatment of the majority of patients who present to Emergency Departments (ED) with severe hypertension. While these patients may present with levels of BP similar to the hypertensive emergency, and may have evidence of target organ involvement, they do not display evidence of ongoing progressive target organ damage. Most of these patients are, in fact, nonadherent to drug therapy or are inadequately treated hypertensive patients and often present to the ED for other reasons. Patients with severe elevations of BP can be managed in the ED with oral agents and appropriate follow-up within 24 hours to several days depending upon the individual characteristics of the patient. It is the correct differentiation of these two forms of hypertensive crises, however, that presents the greatest challenge to the physician.

PREVALENCE

Hypertensive crisis affects upward of 500,000 Americans each year. Although the incidence of hypertensive crisis is low, affecting fewer than 1% of hypertensive adults, more than 50 million Americans suffer from hypertension. Based on the definitions in JNC VI,1 one recent study found that hypertensive crises accounted for more than 25% of all patient visits to the medical section of an ED.2 Hypertensive emergencies accounted for one third of these cases. Although the BP level is not considered a criterion for the diagnosis of a hypertensive emergency, all patients in that study had diastolic BPs exceeding 120 mm Hg. The most prevalent associated complications included cerebral infarction (24.5%), encephalopathy (16.3%), and intracerebral or subarachnoid hemorrhage (4.5%). Acute congestive heart failure with pulmonary edema was seen in 36.8%, acute myocardial infarction or unstable angina in 12%, aortic dissection in 2%, and eclampsia in 4.5%. When considered together, hypertensive crises represented a common presentation to a large city ED. Early triage to establish the appropriate therapeutic strategies for these patients is critical to limiting morbidity and mortality.

SIGNS, SYMPTOMS, AND DIAGNOSIS

Initial Assessment

A brief but thorough history should address the duration as well as the severity of hypertension, all current medications including prescription and nonprescription drugs and, of particular importance, the use of recreational drugs. A history of other comorbid conditions and prior cardiovascular or renal disease is essential to the initial evaluation. Direct questioning regarding the level of compliance with current antihypertensive medications may establish inadequacy of treatment or frank noncompliance.

Frequent or continuous monitoring of BP should be established. Look for historical information suggestive of neurologic, cardiovascular, and/or renal symptoms. Check for specific manifestations such as headache, seizures, chest pain, dyspnea, and edema. The clinical characteristics of a hypertensive emergency are listed in Table 1. The level of BP alone does not determine a hypertensive emergency; rather, it is the degree of target organ involvement that will determine the rapidity with which BP should be reduced to a safer level to prevent or limit target organ damage. Initial therapy will be for a presumptive diagnosis based on the information available during the initial triage evaluation.

The attached algorithm (Table 2) can help the clinician identify those patients who meet the criteria of a hypertensive emergency that requires immediate admission to an ICU for continuous monitoring of BP and initiation of parenteral antihypertensive therapy.3 For patients with uncontrolled hypertension (urgency), evidence of target organ damage may or may not be present but these patients do not demonstrate any evidence of deterioration of target organ function. They can be observed for several hours in the ED during which time their oral medications can be resumed, if discontinued, or if untreated, an oral regimen can be initiated. On occasion, increasing presently inadequate dosages of medication may be appropriate. Appropriate outpatient follow-up can then be arranged within 24 hours to several days as needed, and if no prior evaluation has been performed on this patient for hypertension, an outpatient appointment should be established. Failure to follow-up on this large group of patients is a missed opportunity from the standpoint both of keeping patients in the healthcare system, and establishing optimal BP.

Physical Examination

The physical examination should begin with an assessment of BP, with an appropriate-size cuff in both upper extremities and in a lower extremity if peripheral pulses are markedly reduced. Brachial, femoral, and carotid pulses should be assessed. A careful cardiovascular examination as well as a thorough neurologic examination, including mental status, should be conducted. This assessment will aid in establishing the degree of involvement of affected target organs and should provide clues to the possible existence of a secondary form of hypertension, such as renovascular hypertension. If a secondary cause of hypertension is suspected, appropriate blood and urine samples should be obtained before aggressive therapy is initiated. A careful funduscopic examination should be performed to detect the presence of hemorrhages, exudates, and/or papilledema.

Initial Laboratory Studies

Initial laboratory studies should be limited and rapidly expedited. A urinalysis with microscopic examination of the urinary sediment, an immediate chemistry panel, and an electrocardiogram should be obtained. The urinalysis may reveal significant proteinuria, red blood cells, and/or cellular casts. Cellular casts are suggestive of renal parenchyma disease. Electrolyte abnormalities, particularly hypokalemia or hypomagnesemia, increase the risk of cardiac arrhythmias, and the chemistry panel will also provide evidence of renal and/or hepatic dysfunction. The electrocardiogram should identify evidence of coronary ischemia and/or left ventricular hypertrophy and may reveal pulse deficits, raising the question of aortic dissection. When the clinical examination suggests cerebrovascular ischemia or hemorrhage, or if the patient is comatose, a computed tomographic scan of the head should be immediately obtained.

TREATMENT

Initial Treatment of the Hypertensive Emergency

The initial goal for BP reduction is not to obtain a normal BP but rather to achieve a progressive, controlled reduction in BP to minimize the risk of hypoperfusion in cerebral, coronary, and renovascular beds. Under normal conditions, blood flow to these organs remains relatively constant despite wide fluctuations in BP. In the presence of severe hypertension, the autoregulatory range is shifted upward so that higher levels of BP are tolerated, but organ circulation may be put at risk with sudden reductions in BP. As an example, studies on the autoregulation of cerebral blood flow suggest that the lower limit of autoregulation is about 25% below the resting mean arterial pressure in normotensive subjects and in those with uncomplicated essential hypertension. These observations have led to the suggestion that initial reduction in mean arterial pressure should not exceed 20% to 25% below the pretreatment BP. As an alternative, mean arterial pressure can be reduced within the first 30 to 60 minutes to 110 to 115 mm Hg. If this level of BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24 hours. Excessively rapid reductions in BP have been associated with acute deterioration in renal function, ischemic cardiac or cerebral events, and occasional retinal arterial occlusion and acute blindness.

A significant exception to the above recommendations should be recognized for patients with ischemic stroke, with the awareness that cerebral autoregulation is disrupted in ischemic tissue. There is no clear evidence from clinical trials to support the use of antihypertensive treatment during an acute stroke in the absence of other concurrent disorders such as aortic dissection or heart failure. Antihypertensive treatment may adversely affect cerebral autoregulation in acute stroke. Hypertension associated with an acute ischemic stroke spontaneously decreases to pre-stroke levels within several days.

How Urgent is Urgent Hypertension?

Historically, most patients seen in the ED with severe hypertension did not meet the criteria for hypertensive emergency and were therefore classified as having hypertensive urgencies. Most were treated aggressively in the ED and many were, in fact, admitted to the hospital for control of BP. The important caveat is that elevated blood pressure alone rarely requires emergency therapy. Initial triage should identify those patients who have an elevated BP without any evidence of significant target organ damage or any other impending cardiovascular events, and these patients clearly represent the majority of those seen in the ED. They are often asymptomatic and can be observed for a brief period in the ED to initiate or resume medication in the noncompliant patient or to increase dosages for those being inadequately treated. Follow-up can be arranged within several days in the outpatient department.

The occasional patient who presents to the ED with uncontrolled hypertension and symptoms such as headache, shortness of breath, or epistaxis, may benefit from observation in the ED over a period of several hours and/or an increase in current medications or added medication to further lower BP under observation and monitoring of current symptoms. When clinically stable, the patient may safely be sent home with oral agents and arrangements for follow-up. There are several oral agents available that can provide rapid response in blood pressure within one to several hours. These include agents such as the short-acting ACE inhibitor, captopril, clonidine, Labetalol, or in selected patients the alpha-adrenergic blocking agent prazosin. Some of the pharmacologic characteristics of these oral agents are listed below.

In either case, to discharge the patient from an ED without a confirmed follow-up appointment represents a missed opportunity to get that patient back into treatment for optimal control of BP, which should be a management goal. There is little justification today to admit patients with hypertensive urgency or high BP to a hospital for further evaluation and management when these issues can be efficiently and cost-effectively addressed in the outpatient setting.

Oral Agents for Severe Hypertensive

Several oral agents can be particularly appropriate for treating a hypertensive urgency in the ED.

Captopril, an angiotensin-converting enzyme inhibitor, is well tolerated and can effectively reduce BP in a hypertensive urgency.4 Given by mouth, captopril is usually effective within 15 to 30 minutes and may be repeated in 1 to 2 hours, depending on the response. The drug has been administered sublingually, in which case the onset of action is within 10 to 20 minutes, with a maximal effect reached within 1 hour. Responsiveness to captopril can be enhanced by the coadministration of a loop diuretic such as furosemide. Administration may lead to acute renal failure in patients with high-grade bilateral renal artery stenosis, and some reflex tachycardia may be observed.

Clonidine is a centrally acting alpha-adrenergic agonist with onset of action 30 to 60 minutes after oral administration, and maximal effects are usually seen within 2 to 4 hours. This agent is most commonly administered as a loading dose of 0.1 or 0.2 mg followed by 0.1 mg hourly for several hours until an appropriate BP level is attained. Evidence suggests that a comparable response may be seen with a single 0.2 mg dose.5 The most common adverse effect in the acute setting is drowsiness, affecting up to 45% of patients. Clonidine may be a poor choice when monitoring of mental status is important. Dry mouth is a common complaint, and light-headedness is occasionally observed.

Labetalol, a combined alpha- and beta-adrenergic blocking agent, can be effectively administered orally in a dose of 200 to 400 mg with BP response observed within 2 to 3 hours.6 However, the onset of effect may be observed within 1 to 2 hours. Like other beta-blocking agents, labetalol has the potential to induce heart block and to worsen the symptoms of bronchospasm in the asthmatic patient. Caution must be observed in patients who have more than first-degree heart block, symptomatic bradycardia, or congestive heart failure.

Prazosin is an alpha-adrenergic blocking agent that can have limited benefit in the early management of a patient with a pheochromocytoma. Side effects include first-dose syncope, palpitations, tachycardia, and orthostatic hypotension.

Parenteral Agents for Hypertensive Emergencies

Parental therapy may be initiated in the ED if suitable supervision and monitoring of BP can be provided. More appropriately, the patient should be admitted to an ICU where monitoring of BP is available. A number of parenteral agents are effective in treating hypertensive emergencies (Table 3). Labetalol is effective when administered as 20- to 40-mg bolus intravenous (IV) injections and can provide a step-wise, controlled reduction in BP to a predetermined goal. Once the goal BP is achieved, injections are stopped, and the long duration of action facilitates conversion to effective oral therapy. A continuous infusion of labetalol at 2 mg/min offers an alternative method of administration and is also associated with a gradual yet controlled reduction in BP. Since the beta-blocking effects predominate with this agent, bradycardia or heart block may be observed in patients with intrinsic heart disease.7-9

Sodium nitroprusside has an extremely rapid onset of action, within seconds of initiating an infusion, and a rapid offset of effect within 1 to 2 minutes, which necessitates constant supervision of BP during administration. This agent is particularly effective in reducing preload and afterload in patients with impaired left ventricular function, and a carefully titrated infusion can achieve any desired goal BP. Nitroprusside does not cause sedation or somnolence but is rapidly degraded by light, requiring periodic exchange of solutions.

In patients with significant renal impairment, accumulation of a major metabolite, thiocyanate, may occur over several days with toxic effects. In the presence of poor tissue perfusion and depressed hepatic function, an intermediate metabolite in the form of cyanide can accumulate and occasionally lead to cyanide poisoning.

Nicardipine is an IV form of the dihydropyridine calcium antagonist and is effective in a high percentage of hypertensive emergencies, particularly at higher infusion rates. Its growing popularity can be attributed to its ease of administration. Infusion rates can be increased by 2.5 mg/hr at intervals of 15 to 20 minutes until the maximal recommended dosage of 15 mg/hr is obtained or until the desired reduction in BP is achieved. Dosing of nicardipine is not dependent on body weight. Nicardipine has been shown to reduce both cerebral and coronary ischemia although headache, nausea, and vomiting may occasionally be observed.

Nitroglycerin may be of particular benefit in hypertensive emergencies with coexisting coronary ischemia. Since this agent dilates collateral coronary vessels and, like nitroprusside, has a rapid onset and offset of effect, its use requires close nursing supervision. Unfortunately, at low infusion rates, nitroglycerin has its primary effect on capacitance vessels in which much higher infusion rates are required to effect arteriolar vasodilitation. Infusion rates may be increased at 3- to 5-minute intervals until the desired effect is achieved. Nitroglycerin may be particularly useful in patients with severe coronary ischemia whose BPs are only modestly elevated or in patients with acute hypertension following postcoronary artery bypass surgery. Tolerance to IV nitroglycerin may be observed within 24 to 48 hours of instituting an infusion.

Fenoldapam is a selective, peripheral dopamine1-receptor agonist that induces systemic vasodilation, particularly in the renal circulation.10 This agent also has effects on renal proximal and distal tubules. Fenoldapam does not bind to dopamine2 receptors or beta-adrenergic receptors; it has no alpha-adrenergic agonist effects but is an alpha1 antagonist. This drug does not cross the blood/brain barrier.

Fenoldapam's unique effects on the kidney provide increased urine flow rate, sodium and potassium excretion, and improved creatinine clearance, making this agent particularly attractive in hypertensive emergencies associated with significant renal impairment.

Fenoldapam provides clinical effects similar to those of nitroprusside in improving cardiac hemodynamics in patients with acute congestive heart failure.11 Onset of clinical effect is seen within 5 minutes, and effects tend to dissipate within 30 minutes of discontinuing the infusion. The most common side effects include headache, flushing, tachycardia, and dizziness. A dose-related increase in intraocular pressure has been observed in normotensive and hypertensive patients.12 Inactive metabolites are eliminated in the urine, and no dosage adjustments are required for patients with renal or hepatic impairment.

Hydralazine finds limited use today in pregnant women with preeclampsia. Five to 20 mg may be administered IV as a bolus injection, and may be repeated. The major advantage is this agent's ability to improve uterine blood flow. Hydralazine is contraindicated in patients who have coronary atherosclerosis, as administration is associated with reflex tachycardia and sodium and water retention, together with intense flushing. Headache and increased intracranial pressure have also been observed.

Other Parenteral Agents

Enalaprilat is administered in an IV dose of 1.25 mg and may be repeated at 6-hour intervals. Onset of action is within 30 minutes. Response to enalaprilat in hypertensive emergencies is unpredictable, in part because of variable degrees of plasma volume expansion. This agent may be particularly suitable in hypertensive emergencies associated with congestive heart failure or with high plasma angiotensin II concentrations.

Esmolol is an ultra-short-acting beta-adrenergic blocker that is administered intravenously. Onset of effect is seen within 1 to 5 minutes, with a rapid offset of effect within 15 to 30 minutes after discontinuation. Esmolol may be administered as a 500-µg/kg bolus injection, which may be repeated after 5 minutes. Alternatively, an infusion of 50 to 100 µg/kg/min may be initiated and increased to 300 µg/kg/min as needed. Adverse effects include increased heart block, precipitation of congestive heart failure, and bronchial spasm.

Phentolamine is a nonselective alpha-adrenergic blocking agent that is still used when excess catecholamine states, such as pheochromocytoma, are suspected. It is useful as a diagnostic agent when administered as a bolus injection of 5 to 10 mg in patients with suspected pheochromocytoma. Acute BP lowering will be seen within several minutes and may last 10 to 30 minutes. Tachycardia is common and on occasion may precipitate myocardial ischemia. Nitroprusside and labetalol are more easily titrated in the management of hypertensive emergencies associated with high circulating levels of catecholamines, and therefore phentolamine is rarely used therapeutically today.

Diazoxide is rarely used any longer in the treatment of hypertensive emergencies. Although a potent vasodilator, large doses of 300 mg were often associated with severe hypotension. Smaller miniboluses of 50 mg administered at 10- to 15-minute intervals can provide controlled reduction of BP but are usually associated with reflex tachycardia, hyperglycemia, hyperuricemia, and sodium and water retention. In view of these side effects, diazoxide offers little advantage over several other agents that have more acceptable adverse-effect profiles.

Seizures......Grand mal Vs Petite Mal

[medic429]

From Mayoclinic.com

A grand mal seizure — also known as a tonic-clonic seizure — is a type of seizure characterized by loss of consciousness, falling down, loss of bowel or bladder control, and rhythmic convulsions. Seizures result from an abnormal electrical discharge in the brain. Other types of seizures include petit mal seizure and temporal lobe seizure.

Repeated brain seizures characterize a seizure disorder known as epilepsy. Only a small percentage of people who experience at least a single seizure episode go on to develop epilepsy.

The causes of seizures can vary. Often, the cause is unknown. Sometimes seizures run in families. Finding the underlying cause can help stop seizures.

Petit mal seizure — also known as absence seizure — is a type of seizure that most often occurs in children. An abnormal electrical discharge in the brain causes seizures. Other types of seizures include grand mal seizure and temporal lobe seizure.

Signs and Symptoms

A typical grand mal seizure starts with a loss of consciousness and falling down. This is followed by a 15- to 20-second period with muscle rigidity (tonic phase) and then a one- to two-minute period of violent, rhythmic convulsions (clonic phase). During a grand mal seizure, you may take on a dusky appearance, resulting from decreased blood oxygen levels due to impaired breathing during the seizure.

Most grand mal seizures last from 30 seconds to five minutes. After the seizure, you may experience a headache and drowsiness or confusion. Seizures often occur randomly, though in rare cases, stimulation by light, sound or touch can trigger a seizure in susceptible people. Sleep deprivation and excessive alcohol use also may trigger seizures.

Sometimes the seizures involve only a few muscles, such as one side of the face or one arm or leg. This is called a focal seizure.

Usually, a petit mal seizure involves only a brief, sudden lapse of conscious activity. Each seizure lasts only seconds or minutes, but hundreds may occur each day. During a petit mal seizure, small jerks sometimes occur involving the facial muscles or hands. A person who experiences a petit mal seizure can usually resume normal activities immediately after the seizure ends.

Repeated seizures characterize a seizure disorder known as epilepsy. Only a small percentage of people who have seizures will develop epilepsy. Medications can be effective in eliminating or reducing the number of seizures.

Signs and Symptoms

In a typical petit mal seizure, a brief, sudden absence of consciousness may occur. There may not be any movement at all, only what appears to be staring. In other cases, a seizure may cause:

Lip smacking

Fluttering eyelids

Chewing

Hand movements

Petit mal seizures last only a few seconds. Full recovery is almost instant. Afterward, there is no confusion, but also no memory of the incident.

Petit mal seizures may occur for weeks or months before an adult notices them, because they're so brief. Also, they often occur when a child is sitting quietly and seldom during physical activity.

Because these seizures come and go so quickly, a noticeable decline in a child's learning ability may be the first sign of this disorder. Teachers also may comment about a child's inability to pay attention.

****Respiratory Acidosis?*****

[DwayneEMTP]

I don't pretend to understand this completely, but I wanted to play!

I cut out what I believe to be a brief summary, the complete text can be found at the link below...

http://www.emedicine.com/ped/topic16.htm

Respiratory acidosis occurs when the arterial partial pressure of carbon dioxide (PaCO2) is elevated above the normal range (>44 mm Hg) leading to a blood pH less than 7.35. Respiratory acidosis is not a specific disease. Instead, it is an abnormality resulting from an imbalance between carbon dioxide (CO2) production by the body and excretion by the lungs. This imbalance occurs in severe pulmonary disease, respiratory muscle fatigue, or depressed breathing.

Respiratory acidosis may result from an acute or chronic process. An acute respiratory acidosis can be life-threatening when a sudden and sharp increase in PaCO2 is associated with severe hypoxemia and acidemia. In contrast, chronic respiratory acidosis (>24 h) is characterized by a gradual and sustained increase in PaCO2.

By definition, the diagnosis of respiratory acidosis requires measurement of the arterial PaCO2 and pH. When the diagnosis is made, the cause should be thoroughly investigated.

History:

Does the patient have a history of headaches? With chronic hypercapnia, headaches typically occur at nighttime or when the patient awakens in the morning.

Does the patient have disturbed sleep patterns? Chronic hypercapnia can disturb sleep patterns, leading to a reversed sleep-wake cycle.

Is the patient irritable or anxious, or is he or she having trouble concentrating?

Does the patient have a possible or known exposure to sedatives (eg, narcotics, benzodiazepines, tricyclic antidepressants)? Is the patient recovering from a procedure in which general anesthesia was used?

Does the patient have symptoms of neuromuscular weakness or paralysis?

Bulbar dysfunction suggesting myasthenia gravis

Proximal or distal weakness suggesting a myopathy or Guillain-Barré

Apnea associated with a traumatic injury suggesting an injury to the cervical spinal cord

Does the patient have a long-standing pulmonary disease, such as bronchopulmonary dysplasia, cystic fibrosis, asthma or emphysema?

Does the patient have an acute change in mental status (eg, signs of stroke, postictal state)?

Is the change in mental status associated with a fever, which may suggest encephalitis or meningitis?

Does the patient have signs of increased intracranial pressure (eg, headaches, visual changes, emesis)?

Does the patient have a potential for an anaphylactic reaction?

Does the patient have a potential traumatic mechanism leading to brain injury?

Physical:

Neurologic findings

Early signs are anxiety, disorientation, confusion, and lethargy

Somnolence or coma when PaCO2 greater than 70 mm Hg

Tremor, myoclonus, or asterixis occasionally seen

Brisk deep tendon reflexes (mild–to-moderate respiratory acidosis)

Depressed deep tendon reflexes (severe respiratory acidosis)

Papilledema or blurring of the optic disc

Cardiovascular findings

Tachycardia

Bounding arterial pulses

Hypotension (severe respiratory acidosis or acidemia and hypoxemia)

Skin findings

Warm, flushed, or mottled

Diaphoretic

Respiratory findings

Acute hypercapnia in association with increase work of breathing

Tachypnea, dyspnea, or deep labored breaths

Accessory muscle use and nasal flaring (usually present)

With CNS or peripheral nervous system disease, respiratory distress may not be present

Decreased aeration, crackles, wheezes, or other signs of airway disease

Clubbing, a sign of chronic respiratory disease

Causes:

Extrathoracic airway lesions

Infections - Ludwig angina, laryngotracheobronchitis (croup)

Congenital lesions - Subglottic stenosis, laryngomalacia, craniofacial abnormalities

Thermal airway burns

Tonsillar and adenoidal hypertrophy

Intrathoracic airway obstruction - Asthma, vascular ring

Depression of central respiratory control

Drug induced - Opiates, sedatives, anesthetics, alcohol

Infection - Meningitis, encephalitis

Stroke

Hypoxic encephalopathy

Increased dead space - Wasted ventilation

Pulmonary embolism

Pulmonary vascular disease

Low cardiac output

Acute lung injury

Pneumonia

Pulmonary edema

Lung contusion

Bronchiolitis

Chronic lung disease

Bronchopulmonary dysplasia

Cystic fibrosis

Chronic bronchitis

Chronic obstructive pulmonary disease

Respiratory muscle weakness leading to hypoventilation

Poliomyelitis

Guillain-Barré syndrome

Myasthenia gravis

Muscular dystrophy

Spinal cord injury

Chest wall restriction

Flail chest

Pneumothorax

Pleural effusions

Kyphoscoliosis

Increased CO2 production

Malignant hyperthermia

Extensive burns

I hope this applies..... " Brown-Sequard syndrome"

[itku2er]

Background: Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection of the spinal cord, often in the cervical cord region.

Pathophysiology: The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture comprising fragments of the syndrome or the hemisection syndrome plus additional symptoms and signs is more common. Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

History: Brown-Séquard syndrome may be the result of penetrating injury to the spine, but many other etiologies have been described. Complete hemisection, causing classic clinical features of pure Brown-Séquard syndrome, is rare. Incomplete hemisection causing Brown-Séquard syndrome plus other signs and symptoms is more common.

Physical: Partial Brown-Séquard syndrome is characterized by asymmetric paresis with hypalgesia more marked on the less paretic side. Pure Brown-Séquard syndrome is associated with the following:

Interruption of the lateral corticospinal tracts

Ipsilateral spastic paralysis below the level of the lesion

Babinski sign ipsilateral to lesion

Abnormal reflexes and Babinski sign may not be present in acute injury.

Interruption of posterior white column - Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion

Interruption of lateral spinothalamic tracts: Contralateral loss of pain and temperature sensation. This usually occurs 2-3 segments below the level of the lesion.

Causes:

Spinal cord tumor, metastatic or intrinsic

Trauma, penetrating or blunt

Degenerative disease such as disk herniation and cervical spondylosis

Ischemia

Infectious/inflammatory causes

Meningitis

Empyema

Herpes zoster

Herpes simplex

Myelitis

Tuberculosis

Syphilis

Multiple sclerosis

Hemorrhage, including spinal subdural/epidural and hematomyelia

Prehospital Care: The key to successful prehospital care of patients with Brown-Séquard syndrome is to suspect a cervical or other spinal injury. A low threshold for cervical spine/backboard immobilization is appropriate.

Emergency Department Care:

Care in the ED consists of a thorough evaluation, including neurologic examination for level of injury. Careful cervical spine/dorsal spine immobilization is necessary, with elimination of neck movement.

The nature of sensory loss makes investigation of other injuries more difficult. This mandates thorough and complete physical examination, relying on imaging studies to supplement physical examination.

Consultations:

Neurosurgical or orthopedic consultation is necessary. Practice patterns may dictate involvement of different services.

The goal of pharmacotherapy is to prevent complications.

Drug Category: Corticosteroids -- Multiple studies have demonstrated the improved outcomes of patients with traumatic spinal cord injuries who are given high-dose steroids early in the clinical course.Drug Name

Methylprednisolone (Solu-Medrol, Depo-Medrol) -- Decreases inflammation by suppressing polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult Dose 30 mg/kg IV bolus over 15 min, then 5.4 mg/kg/h infusion for 23 h; should be initiated within 8 h of injury

Pediatric Dose Administer as in adults (NACSIS study enrolled patients as young as 13 y)

Contraindications Documented hypersensitivity; viral, fungal, or tubercular skin infections

Interactions Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Slightly higher rates of wound infection and GI bleeding in methylprednisolone group in the NACSIS study (not statistically significant); other possible complications include hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections

Prognosis:

Prognosis for Brown-Séquard syndrome is poor and depends to a large degree on the etiology of the syndrome. Early treatment with high-dose steroids has shown benefit.

Interesting I liked that one..... Hemmorrhagic shock vs cardiogenic shock

[medic001918]

Quick simple terms, heorrhagic shock would be the inability to maintain adequate perfusion secondary to a fluid volume loss where cadiogenic shock would be the inability to provide perfusion due to a lack of an effective heart (or pump). While the two conditions may sometimes present similar, the history of the event is usually helpful in distinguishing the two and requires two different treatment modalities.

Hemorrhagic Shock...from emedicine.com once again.

Background: Shock is a state in which adequate perfusion to sustain the physiologic needs of organ tissues is not present. Many conditions, including sepsis, blood loss, impaired autoregulation, and loss of autonomic tone, may produce shock or shocklike states.

Pathophysiology: In hemorrhagic shock, blood loss exceeds the body's ability to compensate and provide adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be caused by spontaneous hemorrhage (eg, GI bleeding, childbirth), surgery, and other causes.

Most frequently, clinical hemorrhagic shock is caused by an acute bleeding episode with a discrete precipitating event. Less commonly, hemorrhagic shock may be seen in chronic conditions with subacute blood loss.

Physiologic compensation mechanisms for hemorrhage include initial peripheral and mesenteric vasoconstriction to shunt blood to the central circulation. This is then augmented by a progressive tachycardia. Invasive monitoring may reveal an increased cardiac index, increased oxygen delivery (ie, DO2), and increased oxygen consumption (ie, VO2) by tissues. Lactate levels, the acid-base status, and other markers also may provide useful indicators of physiologic status. Age, medications, and comorbid factors all may affect a patient's response to hemorrhagic shock.

Failure of compensatory mechanisms in hemorrhagic shock can lead to death. Without intervention, a classic trimodal distribution of deaths is seen in severe hemorrhagic shock. An initial peak of mortality occurs within minutes of hemorrhage due to immediate exsanguination. Another peak occurs after 1 to several hours due to progressive decompensation. A third peak occurs days to weeks later due to sepsis and organ failure.

Frequency:

* In the US: Accidental injuries are the leading cause of death in individuals aged 1-44 years.

History: History taking should address the following:

* Specific details of the mechanism of trauma or other cause of hemorrhage are essential.

* Inquire about a history of bleeding disorders and surgery.

* Prehospital interventions, especially the administration of fluids administered, and changes in vital signs should be determined. Emergency medical technicians or paramedics should share this information.

Physical: Findings at physical examination may include the following:

* Head, ears, eyes, nose, and throat

o Sources of hemorrhage usually are apparent.

o The blood supply of the scalp is rich and can produce significant hemorrhage.

o Intracranial hemorrhage usually is insufficient to produce shock, except possibly in very young individuals.

* Chest

o Hemorrhage into the thoracic cavities (pleural, mediastinal, pericardial) may be discerned at physical examination. Ancillary studies often are required for confirmation.

o Signs of hemothorax may include respiratory distress, decreased breath sounds, and dullness to percussion.

o Tension hemothorax, or hemothorax with cardiac and contralateral lung compression, produces jugular venous distention and hemodynamic and respiratory decompensation.

o With pericardial tamponade, the classic triad of muffled heart sounds, jugular venous distention, and hypotension often is present, but these signs may be difficult to appreciate in the setting of an acute resuscitation.

* Abdomen

o Injuries to the liver or spleen are common causes of hemorrhagic shock.

o Blood irritates to the peritoneal cavity; diffuse tenderness and peritonitis are common when blood is present. However, the patient with altered mental status or multiple concomitant injuries may not have the classic signs and symptoms at physical examination.

o Progressive abdominal distention in hemorrhagic shock is highly suggestive of intraabdominal hemorrhage.

* Pelvis

o Fractures can produce massive bleeding. Retroperitoneal bleeding must be suspected.

o Flank ecchymosis may indicate retroperitoneal hemorrhage.

* Extremities

o Hemorrhage from extremity injuries may be apparent, or tissues may obscure significant bleeding.

o Femoral fractures may produce significant blood loss.

* Nervous system

o Agitation and combativeness may be seen in the initial stages of hemorrhagic shock.

o These signs are followed by a progressive decline in level of consciousness due to cerebral hypoperfusion or concomitant head injury.

Lab Studies:

* Laboratory studies are essential in management of many forms of hemorrhagic shock. Baseline levels are determined frequently, but these infrequently change the initial management after trauma. Serial evaluations of the following can help guide ongoing therapy.

o CBC

o Prothrombin time and/or activated partial thromboplastin time

o Urine

o ABGs (Levels reflect acid-base and perfusion status.)

* Lactate and base deficit are used in some centers.

* Typed and crossmatch packed red blood cells should be obtained immediately.

* Fresh frozen plasma and platelets also may be required to correct coagulopathies that develop in severe hemorrhagic shock.

Imaging Studies:

* Standard radiography

o Cervical spine, chest, and pelvis radiographs are the standard screening images for severe trauma.

o Other radiographs may be indicated for orthopedic injuries.

* Computed tomography

o Image the appropriate for region of suspected injury.

o CT scanning frequently is the method of choice for evaluating possible intra-abdominal and/or retroperitoneal sources of hemorrhage in stable patients.

o Oral contrast material may not increase the diagnostic yield of abdominal CT scanning in blunt trauma. Scanning should not be delayed to administer oral contrast material.

* Ultrasonography

o Bedside abdominal ultrasonography can be useful for the rapid detection of free intra-abdominal fluid and, sometimes, specific parenchymal injury.

o Thoracic ultrasonographic findings can immediately confirm hemothorax or pericardial tamponade.

* Directed angiography may be diagnostic and therapeutic. Interventional radiologists have had good success achieving hemostasis in hemorrhage caused by a variety of vessels and organs.

Other Tests:

* An ECG can be useful for detecting dysrhythmias and cardiac sequelae of shock.

Procedures:

* Tube thoracostomy is necessary in hemothorax and hemothorax with or without pneumothorax.

* Central venous access facilitates fluid resuscitation and monitoring of central venous pressure and is necessary if peripheral intravenous access is inadequate or impossible to obtain.

* Diagnostic peritoneal lavage is used to detect intra-abdominal blood, fluid, and intestinal contents. It is sensitive but not specific for abdominal injury. It is not used to evaluate the retroperitoneum, which can hold significant hemorrhage, and does not identify the source of hemorrhage.

Prehospital Care:

* The standard care consists of rapid assessment and expeditious transport to an appropriate center for evaluation and definitive care.

* Intravenous access and fluid resuscitation are standard. However, this practice has become controversial.

o For many years, aggressive fluid administration has been advocated to normalize hypotension associated with severe hemorrhagic shock. Recent studies of urban patients with penetrating trauma have shown that mortality increases with these interventions; these findings call these practices into question.

o Reversal of hypotension prior to the achievement of hemostasis may increase hemorrhage, dislodge partially formed clots, and dilute existing clotting factors. Findings from animal studies of uncontrolled hemorrhage support these postulates. These provocative results raise the possibility that moderate hypotension may be physiologically protective and should be permitted, if present, until hemorrhage is controlled.

o These findings should not yet be clinically extrapolated to other settings or etiologies of hemorrhage. The ramifications of permissive hypotension in humans remain speculative, and safety limits have not been established yet.

Emergency Department Care:

* Management of hemorrhagic shock should be directed toward optimizing perfusion of and oxygen delivery to vital organs.

* Diagnosis and treatment of the underlying hemorrhage must be performed rapidly and concurrently with management of shock.

* Supportive therapy, including oxygen administration, monitoring, and establishment of intravenous access (eg, 2 large-bore catheters in peripheral lines, central venous access) should be initiated.

o Intravascular volume and oxygen-carrying capacity should be optimized.

o In addition to crystalloids, some colloid solutions, hypertonic solutions, and oxygen-carrying solutions (eg, hemoglobin-based and perfluorocarbon emulsions) are used or being investigated for use in hemorrhagic shock.

o Blood products may be required.

* Determination of the site and etiology of hemorrhage is critical to guide further interventions and definitive care.

* Control of hemorrhage may be achieved in the ED, or control may require consultations and special interventions.

Consultations: Consult a general or specialized surgeon, gastroenterologist, obstetrician-gynecologist, radiologist, and others as required

Cardiogenic Shock taken from emedicine as well for continuity.

Background: Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI).

Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [bP] less than 90 mm Hg lasting more than 30 min) with evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure (Hochman, 1999). Tissue hypoperfusion was defined as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both.

Pathophysiology: The most common initiating event in cardiogenic shock is AMI. Dead myocardium does not contract, and classical teaching has been that when more than 40% of the myocardium is irreversibly damaged (particularly, the anterior cardiac wall), cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilatation, and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. The SHOCK trial, however, demonstrated that left ventricular ejection fraction is not always depressed in the setting of cardiogenic shock. Additional surprising findings included nonelevated systemic vascular resistance on vasopressors and that most survivors have only New York Heart Association (NYHA) class I congestive heart failure.

A systemic inflammatory response syndrome–type mechanism has been implicated in the pathophysiology of cardiogenic shock. Elevated levels of white blood cells, body temperature, complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during myocardial stress. iNOS induces nitric oxide production, which may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the expression of interleukins, which may themselves cause hypotension.

Myocardial ischemia causes a decrease in contractile function, which leads to left ventricular dysfunction and decreased arterial pressure; these, in turn, exacerbate the myocardial ischemia. The end result is a vicious cycle that leads to severe cardiovascular decompensation. Other pathophysiological mechanisms responsible for cardiogenic shock include papillary muscle rupture leading to acute mitral regurgitation (4.4%); decreased forward flow, ejection fraction, and ventricular septal defect (1.5%); and free wall rupture (4.1%) as a consequence of AMI.

Right ventricular (RV) infarct, by itself, may lead to hypotension and shock because of reduced preload to the left ventricle. The management of RV infarcts is discussed elsewhere but should be considered in the setting of inferior wall MI.

Cardiac tamponade may result as a consequence of pericarditis, uremic pericardial effusion, or in rare cases systemic lupus erythematosus.

Whenever patients who present in shock have been exposed to medications that may cause hypotension, these drugs should be considered as possible culprits in the disease. Calcium channel blockers may cause profound hypotension with a normal or elevated heart rate. Beta-blocking agents may also cause hypotension. Hypotension can be seen with or without bradycardia, or AV node block can be seen with either of these types of medications. If these medications are the culprits, therapy directed at these toxicities is beneficial. Nitroglycerin, angiotensin-converting enzyme inhibitors, opiate, and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic shock.

Initiating events other than AMI and ischemia include infection, drug toxicity, and pulmonary embolus.

Frequency:

* In the US: Cardiogenic shock occurs in 8.6% of patients with ST-segment elevation MI with 29% of those presenting to the hospital already in shock. It occurs only in 2% of non–ST-segment elevation MI.

Mortality/Morbidity: Cardiogenic shock is the leading cause of death in AMI.

* The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For those younger than 75 years, the mortality rate is 39.5%.

* Outcomes significantly improve only when rapid revascularization can be achieved. The recent SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not attempted, mortality rates approach 70%.

* Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy), but they have been reported to be as low as 30-50%.

Race:

* Race-stratified mortality rates are as follows: Hispanics, 74%; African Americans, 65%; whites, 56%; and Asians/others, 41%.

* Race-based differences in mortality disappear with revascularization.

Sex: Women comprise 42% of all cardiogenic shock patients.

History: Most patients with cardiogenic shock have an AMI and, therefore, present with the constellation of symptoms of acute cardiac ischemia (eg, chest pain, shortness of breath, diaphoresis, nausea, vomiting). Patients experiencing cardiogenic shock also may present with pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms.

Physical: The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs.

* Although the patient may eventually require endotracheal intubation, the airway usually is patent initially.

* Breathing may be labored, with audible coarse crackles or wheezing.

* As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings.

* Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present.

* Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring.

* Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure.

* LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing.

* Careful cardiac examination may reveal mechanical causes of cardiogenic shock.

o Loud murmurs may indicate a valvular dysfunction, whereas muffled heart tones with jugular venous distention and pulsus paradoxus may suggest tamponade (Beck triad).

o A gallop may also be heard. The presence of an S3 heart sound is pathognomonic of congestive heart failure. The presence of pulmonary edema increases the likelihood of cardiogenic shock in the setting of hypotension.

Causes: The vast majority of cases of cardiogenic shock are due to acute myocardial ischemia.

* Mechanisms not related to acute infarction include the following:

o Systolic - Beta-blocker overdose, calcium channel blocker overdose, myocardial contusion, respiratory acidosis, hypocalcemia, hypophosphatemia, and cardiotoxic drugs (eg, doxorubicin [Adriamycin])

o Diastolic - Ventricular hypertrophy and restrictive cardiomyopathies

o After load - Aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow obstruction, aortic coarctation, and malignant hypertension

o Valvular/structural - Mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma or thrombus, and tamponade

* Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), and dysrhythmia.

Lab Studies:

* No one test is completely sensitive or specific for cardiogenic shock. Laboratory studies are directed at the potential underlying cause.

* In most cases, the usual workup includes tests of all of the following, which usually are assessed in cases of suspected cardiac ischemia:

o Cardiac enzymes (eg, creatine kinase, troponin, myoglobin)

o CBC

o Electrolytes

o Coagulation profile (eg, prothrombin time, activated partial thromboplastin time)

o An ABG may be useful to evaluate acid-base balance because acidosis can have a particularly deleterious effect on myocardial function. Elevated serum lactate level is an indicator of shock.

o Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure and as an independent prognostic indicator of survival. A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension; however, an elevated BNP level does not rule in the disease.

Imaging Studies:

* A portable chest radiograph is helpful because it gives an overall impression of the cardiac size, pulmonary vascularity, and coexistent pulmonary pathology, and it provides a rough estimate of mediastinal and aortic sizes in the event that an aortic etiology is being considered.

Other Tests:

* An ECG is helpful if it reveals an acute injury pattern consistent with an AMI. A normal ECG, however, does not rule out the possibility. ECGs are often most helpful when they can be compared with previous tracings.

* An echocardiogram obtained in the ED can be extremely useful.

o It may be diagnostic and reveal akinetic or dyskinetic areas of ventricular wall motion.

o It may reveal surgically correctable causes, such as valvular dysfunction and tamponade.

Procedures:

* Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure and pulmonary capillary wedge pressure. Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which LV preload is difficult to determine. Central venous pressure may also be used to guide fluid resuscitation. Cardiogenic shock may be indicated by a cardiac index of less than 1.8 L/min/m2 with a pulmonary capillary wedge pressure greater than 18 mm Hg.

* An intra-aortic balloon pump may be placed in the ED as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) to decrease myocardial workload and to improve end-organ perfusion.

Prehospital Care: Prehospital care is aimed at minimizing any further ischemia and shock.

* All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring.

* Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED physician, can thus be alerted, and may mobilize the appropriate resources.

* Inotropic medications should be considered in systems with appropriately trained paramedical personnel.

Emergency Department Care: ED care is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory. The ED physician should be alert to the fact that the SHOCK trial demonstrated that PCI or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best.

Treatment begins with assessment and management of the ABCs.

* The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen.

* Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure or pulmonary capillary wedge pressure monitoring.

* Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart.

o Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption.

o Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload.

o Natrecor (nesiritide) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.

o Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock.

* The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow. Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use.

Consultations: Consult a cardiologist at the earliest opportunity because his or her insight and expertise may be invaluable for facilitating echocardiographic support, placement of an IABP, and transfer to more definitive care (eg, cardiac catheterization suite, intensive care unit, operating room).

***And now onto the next topics, how about a triad of triads? Cushings triad? Beck's triad? And the classical triad as it applies to OB calls?***

Shane

NREMT-P

[Ace844]

And now onto the next topics, how about a triad of triads? Cushings triad? Beck's triad? And the classical triad as it applies to OB calls?***

Cushing's triad

Cushing's triad is the triad of hypertension, bradycardia, and Cheyne-Stokes respiration (irregular breathing) in patients with head injuries. It is named after Harvey Williams Cushing (1869-1939), the American neurosurgeon who first described this combination of signs.

Identification of the combination of these signs is critically important, especially in the setting of emergency medicine because it is a sign of increasing intracranial pressure. A patient with these signs will usually require urgent life-saving surgery which may include drilling a burr hole into the head to release intracranial pressure.

Clues in Respiratory Patterns:

Distinct patterns such as Cheyne-Stokes breathing, central neurogenic hyperventilation, or Biot's breathing may indicate specific areas of trauma. Normal breathing, however, does not rule out the presence of a small, unilateral lesion.Cheyne-Stokes breathing is seen with bihemispheric lesions or lesions in the basal ganglia. Central neurogenic hyperventilation, or sustained hyperventilation with respiratory rates greater than 40 per minute, is associated with lower midbrain or upper pontine injury. It must be distinguished from hyperventilation due to other common causes including hypoxia, acidosis, sepsis, drug toxicities, and anxiety.Biot's breathing is an irregular or ataxic type of respiration. Breathing is chaotic with loss of regularity in the pace and depth of inspiration and expiration. It is seen with pontine or medullary dysfunction due to trauma.In addition to abnormal breathing patterns, brain injury may also cause repetitive respiratory reflexes (sighing, yawning, hiccups), suggesting suppression of higher cortical function. These signs may also warn of impending herniation

Hemodynamics and Intracranial Pressure in Head Trauma:

Cerebral blood flow is maintained by cardiac output (heart rate multiplied by stroke volume), cerebral perfusion pressure (mean arterial pressure minus intracranial pressure), and autoregulation. Autoregulation is the intrinsic ability of cerebral blood vessels to constrict or dilate in response to changes in mean arterial pressure. Disruption of autoregulation leads to an increased risk of cerebral ischemia if blood pressure falls and to disruption of the blood-brain barrier if blood pressure rises. In turn, disruption of the blood-brain barrier causes extravasation of protein and transudation of water, leading to cerebral edema.

Cushing's triad, which includes bradycardia, hypertension (with widened pulse pressure), and a change in respiratory pattern, is seen in head injuries with increased intracranial pressure (ICP).

Head injuries rarely cause hypotension, except in spinal cord injuries (hypotension with bradycardia); therefore, other causes of hypotension must be sought.

Normal ICP ranges from 0 to 15 mm Hg, depending on the total volume of brain tissue and the total volume of cerebrospinal fluid (CSF). Normal fluctuations in ICP are due to translocation of CSF into the subarachnoid space and to increased CSF absorption.

Possible triggers of a transient ICP increase in the clinical setting include prone positioning, suctioning, painful procedures, coughing, straining, REM sleep, and abnormal respiratory patterns. A sustained rise in ICP is seen when any added volume (mass, blood, abscess, cerebral edema) exceeds compensatory mechanisms. The magnitude of the increase depends on the amount and accumulation rate of the additional volume and the total volume of the intracranial cavity. The adverse effects of increased ICP are due to reduced cerebral blood flow, brain shift, and distortion. Signs and symptoms of increased ICP in addition to Cushing's triad include headache, vomiting, drowsiness, and lethargy. Studies have shown that common practices aimed at lowering ICP, such as intubation and hyperventilation, are often futile.

Cerebral edema is not uncommon after head injuries. The cause may be cytotoxic, vasogenic, or ischemic. Cytotoxic edema is associated with neuronal degeneration. Each neuron is equipped with a sodium pump to maintain fluid and electrolyte balance. Traumatic injury can cause dysfunction of this pump and consequent influx of sodium and water into the cells. Vasogenic edema is due to compromise of the blood-brain barrier by damaged capillaries that allow plasma leakage into brain tissue. Ischemic edema is due to a combination of cytotoxic and vasogenic processes.

Cerebral edema is the major cause of reduced blood flow to the brain. It is also a major contributor to increased ICP. Cerebral edema occurs between 1 and 18 hours after injury, peaking at day 3. Alcohol promotes cerebral edema by increasing the permeability of the blood-brain barrier. Common radiographic signs include small or absent sulci, low attenuation within adjacent white matter, compression of the ventricles, and poor gray-white differentiation.

The combination of increased ICP and cerebral edema with an expanding lesion is the cause of various herniation syndromes. The most common is tentorial herniation, in which the uncus of the temporal lobe is pushed over the edge of the tentorial notch. Typical findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III. With compression of the midbrain as herniation progresses, patients will also have a decreased level of consciousness. Projectile vomiting is common. If the cerebral peduncles are also compressed, patients may display contralateral posturing. Patients have also been described as having Cheyne-Stokes respirations or central neurogenic hyperventilation.

A variant worth noting is cerebellar tonsil herniation syndrome, meaning that the cerebellar tonsils are being forced through the foramen magnum. This syndrome is usually associated with lesions in the posterior fossa. Respiratory arrest ensues as the respiratory centers are compressed in the medulla.

Cushing's law

Also known as:

Cushing's effect

Cushing's phenomenon

Cushing's reaction

Cushing's response

Harvey Williams Cushing

American neurosurgeon, born April 8, 1869, Cleveland, Ohio; died October 7, 1939, New Haven, Connecticut.

Description:

An acute increase of intracranial pressure also causes compression of the cerebral blood vessels and cerebral ischemia, producing an increase of systemic blood pressure over the vasomotor centre, with simultaneous reduction in heart rate, respiratory slowing.

Bibliography:

H. W. Cushing:

Some experimental and clinical observations concerning states of increased intracranial tension.

American Journal of the Medical Sciences, Thorofare, N.J., 1902, 124: 375-400.

http://www.emedicine.com/emerg/topic412.htm

Becks Triad

Becks Triad is the clinical presentation of Cardiac Tamponade. In a nut shell cardiac tamponade occurs when blood accumulates in the pericardial sac (surrounding the heart). This is more commonly the result from trauma to the heart i.e stab wound or even an acute M.I. Blood fills the pericardial sac which in turn reduces the ability of the heart to pump effectively. This is because the ventricles are prevented from filling due to pressure. Prevention of ventricular filling causes a decrease in stroke volume and a fall in BLOOD PRESSURE (one sign). Due to the accumulation of blood in the cavity if you listen with a stethoscope the heart signs are MUFFLED (two signs). An impaired ability of the ventricles to fill with blood causes blood to back up behind the right ventricle and more commonly than not the neck veins become distended hence ELEVATED VENOUS PRESSURE.

There you go becks triad -

1) Muffled heart sounds

2) Falling blood pressure

3) Elevated venous pressure

Not sure about this one

the classical triad as it applies to OB calls?

"medic;" Did you mean female athlete triad syndrome, adie syndrome, Currarino's?

ACE844

[medic001918]

The classic triad as it applies to ectopic pregnancy. While the triad is only about 100% reliable (something that I learned by looking it up again for this thread), prehospitally this could be useful to provide a potentital differential diagnosis. Great information on the first two Ace. Strong work as usual.

*The part about the triad is highlighted in bold*

Ectopic pregnancy presents a major health problem for women of childbearing age. It is the result of a flaw in human reproductive physiology that allows the conceptus to implant and mature outside the endometrial cavity, which ultimately ends in death of the fetus. Without timely diagnosis and treatment, ectopic pregnancy can become a life-threatening situation.

Ectopic pregnancy currently is the leading cause of pregnancy-related death during the first trimester in the United States, accounting for 9% of all pregnancy-related deaths. In addition to the immediate morbidity caused by ectopic pregnancy, the woman's future ability to reproduce may be adversely affected as well.

History of the Procedure: Ectopic pregnancy was first described in the 11th century, and, until the middle of the 18th century, it was usually fatal. John Bard reported the first successful surgical intervention to treat an ectopic pregnancy in New York City in 1759.

The survival rate in the early 19th century was dismal. One report demonstrated only 5 patients of 30 surviving the abdominal operation. Interestingly, the survival rate in patients who were left untreated was 1 of 3.

In the beginning of the 20th century, great improvements in anesthesia, antibiotics, and blood transfusion contributed to the decrease in the maternal mortality rate. In the early half of the 20th century, 200-400 deaths per 10,000 cases were attributed to ectopic pregnancy. In 1970, the Centers for Disease Control and Prevention (CDC) began to record the statistics regarding ectopic pregnancy, reporting 17,800 cases. By 1992, the number of ectopic pregnancies had increased to 108,800. Concurrently, however, the case-fatality rate decreased from 35.5 deaths per 10,000 cases in 1970 to 2.6 per 10,000 cases in 1992.

Problem: Ectopic pregnancy is derived from the Greek word ektopos, meaning out of place, and it refers to the implantation of a fertilized egg in a location outside of the uterine cavity, including the fallopian tubes, cervix, ovary, cornual region of the uterus, and the abdominal cavity. This abnormally implanted gestation grows and draws its blood supply from the site of abnormal implantation. As the gestation enlarges, it creates the potential for organ rupture because only the uterine cavity is designed to expand and accommodate fetal development. Ectopic pregnancy can lead to massive hemorrhage, infertility, or death.

Frequency: Since 1970, the frequency of ectopic pregnancy has increased 6-fold, and it now occurs in 2% of all pregnancies. An estimated 108,800 ectopic pregnancies in 1992 resulted in 58,200 hospitalizations with an estimated cost of $1.1 billion.

Etiology: Multiple factors contribute to the relative risk of ectopic pregnancy. In theory, anything that hampers the migration of the embryo to the endometrial cavity could predispose women to ectopic gestation. The most logical explanation for the increasing frequency of ectopic pregnancy is previous pelvic infection; however, most patients presenting with an ectopic pregnancy have no identifiable risk factor. The following risk factors have been linked with ectopic pregnancy:

Pelvic inflammatory disease

The most common cause is antecedent infection caused by Chlamydia trachomatis. Patients with chlamydial infection have a range of clinical presentations, from asymptomatic cervicitis to salpingitis and florid pelvic inflammatory disease (PID). More than 50% of women who have been infected are unaware of the exposure. Other organisms causing PID, such as Neisseria gonorrhoeae, increase the risk of ectopic pregnancy. A history of salpingitis increases the risk of ectopic pregnancy 4-fold. The incidence of tubal damage increases after successive episodes of PID (ie, 13% after 1 episode, 35% after 2 episodes, 75% after 3 episodes).

History of prior ectopic pregnancy

After one ectopic pregnancy, a patient incurs a 7- to 13-fold increase in the likelihood of another ectopic pregnancy. Overall, a patient with prior ectopic pregnancy has a 50-80% chance of having a subsequent intrauterine gestation, and a 10-25% chance of a future tubal pregnancy.

History of tubal surgery and conception after tubal ligation

Prior tubal surgery has been demonstrated to increase the risk of developing ectopic pregnancy. The increase depends on the degree of damage and the extent of anatomic alteration. Surgeries carrying higher risk of subsequent ectopic pregnancy include salpingostomy, neosalpingostomy, fimbrioplasty, tubal reanastomosis, and lysis of peritubal or periovarian adhesions.

Conception after previous tubal ligation increases a women's risk of developing ectopic pregnancies. Thirty-five to 50% of patients who conceive after a tubal ligation are reported to experience an ectopic pregnancy. Failure after bipolar tubal cautery is more likely to result in ectopic pregnancy than occlusion using suture, rings, or clips. Failure is attributed to fistula formation that allows sperm passage. Ectopic pregnancies following tubal sterilizations usually occur 2 or more years after sterilization, rather than immediately after. In the first year, only about 6% of sterilization failures result in ectopic pregnancy.

Use of fertility drugs or assisted reproductive technology

Ovulation induction with clomiphene citrate or injectable gonadotropin therapy has been linked with a 4-fold increase in the risk of ectopic pregnancy in a case-control study. This finding suggests that multiple eggs and high hormone levels may be significant factors.

One study has demonstrated that infertility patients with luteal phase defects have a statistically higher ectopic pregnancy rate than patients whose infertility is caused by anovulation. The risk of ectopic pregnancy and heterotopic pregnancy (ie, pregnancies occurring simultaneously in different body sites) dramatically increases when a patient has used assisted reproductive techniques to conceive, such as in vitro fertilization (IVF) or gamete intrafallopian transfer (GIFT). In a study of 3000 clinical pregnancies achieved through in vitro fertilization, the ectopic pregnancy rate was 4.5%, which is more than double the background incidence. Furthermore, studies have demonstrated that up to 1% of pregnancies achieved through IVF or GIFT can result in a heterotopic gestation, compared to an incidence of 1 in 30,000 pregnancies for spontaneous conceptions.

Use of an intrauterine device

The presence of an inert copper-containing or progesterone intrauterine device (IUD) traditionally has been thought to be a risk factor for ectopic pregnancy. However, only the progesterone IUD has a rate of ectopic pregnancy higher than that for women not using any form of contraception. The modern copper IUD does not increase the risk of ectopic pregnancy. Nevertheless, if a woman ultimately conceives with an IUD in place, it is more likely to be an ectopic pregnancy. The actual incidence of ectopic pregnancies with IUD use is 3-4%.

Increasing age

The highest rate of ectopic pregnancy occurs in women aged 35-44 years. A 3- to 4-fold increase in the risk for developing an ectopic pregnancy exists compared to women aged 15-24 years. One proposed explanation involves the myoelectrical activity in the fallopian tube, which is responsible for tubal motility. Aging may result in a progressive loss of myoelectrical activity along the fallopian tube.

Smoking

Cigarette smoking has been shown to be a risk factor for developing an ectopic pregnancy. Studies have demonstrated elevated risk ranging from 1.6-3.5 times that of nonsmokers. A dose-response effect also has been suggested. Based on laboratory studies in humans and animals, researchers have postulated several mechanisms by which cigarette smoking might play a role in ectopic pregnancies. These mechanisms include one or more of the following: delayed ovulation, altered tubal and uterine motility, or altered immunity. To date, no study has supported a specific mechanism by which cigarette smoking affects the occurrence of ectopic pregnancy.

Salpingitis isthmica nodosum

Salpingitis isthmica nodosum is defined as the microscopic presence of tubal epithelium in the myosalpinx or beneath the tubal serosa. These pockets of epithelium protrude through the tube, similar to small diverticula. Studies of serial histopathological sections of the fallopian tube have revealed that approximately 50% of patients treated with salpingectomy for ectopic pregnancy have evidence of salpingitis isthmica nodosum. The etiology of salpingitis isthmica nodosum is unclear, but proposed mechanisms include postinflammatory and congenital as well as acquired tubal changes such as observed with endometriosis.

Other

Other risk factors associated with increased incidence of ectopic pregnancy include previous diethylstilbestrol (DES) exposure, a T-shaped uterus, prior abdominal surgery, failure with progestin-only contraception, and ruptured appendix.

Pathophysiology: Most ectopic pregnancies are located in the fallopian tube (see Image 1). The most common site is the ampullary portion of the tube, where over 80% occur. The next most common sites are the isthmic segment of the tube (12%), the fimbria (5%), and the cornual and interstitial region of the tube (2%). Nontubal sites of ectopic pregnancy are a rare occurrence, with abdominal pregnancies accounting for 1.4% of ectopic pregnancies and ovarian and cervical sites accounting for 0.2% each.

Clinical: The classic clinical triad of ectopic pregnancy is pain, amenorrhea, and vaginal bleeding. Unfortunately, only 50% of patients present typically. Patients may present with other symptoms common to early pregnancy, including nausea, breast fullness, fatigue, low abdominal pain, heavy cramping, shoulder pain, and recent dyspareunia. Astute clinicians should have a high index of suspicion for ectopic pregnancy in any woman who presents with these symptoms and who presents with physical findings of pelvic tenderness, enlarged uterus, adnexal mass, or tenderness.

Remember, however, that only 40-50% of patients with an ectopic pregnancy present with vaginal bleeding, 50% have a palpable adnexal mass, and 75% may have abdominal tenderness. Approximately 20% of patients with ectopic pregnancies are hemodynamically compromised at initial presentation, which is highly suggestive of rupture. Fortunately, using modern diagnostic techniques, most ectopic pregnancies may be diagnosed prior to rupturing.

Numerous conditions may have a presentation similar to an extrauterine pregnancy. The most common of these are appendicitis, salpingitis, ruptured corpus luteum cyst or ovarian follicle, spontaneous abortion or threatened abortion, ovarian torsion, and urinary tract disease. Intrauterine pregnancies with other abdominal or pelvic problems such as degenerating fibroids must also be included in the differential diagnosis.

Medical therapy

Medical therapy involving methotrexate may be indicated in certain patients. A number of factors must be considered. The patient must be hemodynamically stable, with no signs or symptoms of active bleeding or hemoperitoneum. Furthermore, she must be reliable, compliant, and able to return for follow-up. Another factor is size of the gestation, which should not exceed 3.5 cm at its greatest dimension on ultrasound (US) measurement. She should not have any contraindications to the use of methotrexate.

Surgical therapy

Within the last 2 decades, a more conservative surgical approach to unruptured ectopic pregnancy using minimally invasive surgery has been advocated to preserve tubal function (see Surgical therapy). Laparoscopy has become the recommended approach in most cases. Laparotomy is usually reserved for patients who are hemodynamically unstable or patients with cornual ectopic pregnancies. It also is a preferred method for surgeons inexperienced in laparoscopy and in patients where laparoscopic approach is difficult (eg, secondary to the presence of multiple dense adhesions, obesity or massive hemoperitoneum). In a patient who has completed childbearing and no longer desires fertility, in a patient with a history of an ectopic pregnancy in the same tube, or in a patient with severely damaged tubes, total salpingectomy is the procedure of choice.

Expectant management

Candidates for successful expectant management are asymptomatic and have no evidence of rupture or hemodynamic instability. Furthermore, they should portray objective evidence of resolution, such as declining bhCG levels. They must be fully compliant and must be willing to accept the potential risks of tubal rupture.

Now let's have someone find some information on RHABDOMYOLYSIS!!! And some extra credit for disseminated intravascular coagulation. Had to mention that one before I forgot about it.

Shane

NREMT-P

[PRPGfirerescuetech]

Mwahahahaha...i actually saw this dx once...

Definition

Rhabdomyolysis is the breakdown of muscle fibers resulting in the release of muscle fiber contents into the circulation. Some of these are toxic to the kidney and frequenty result in kidney damage.

Causes, incidence, and risk factors

Myoglobin is an oxygen-binding protein pigment found in the skeletal muscle. When the skeletal muscle is damaged, the myoglobin is released into the bloodstream. It is filtered out of the bloodstream by the kidneys. Myoglobin may occlude the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure.

Myoglobin breaks down into potentially toxic compounds, which will also cause kidney failure. Necrotic (dead tissue) skeletal muscle may cause massive fluid shifts from the bloodstream into the muscle, reducing the relative fluid volume of the body and leading to shock and reduced blood flow to the kidneys.

The disorder may be caused by any condition that results in damage to skeletal muscle, especially trauma.

Risk factors include the following:

* Severe exertion such as marathon running or calisthenics

* Ischemia or necrosis of the muscles (as may occur with arterial occlusion, deep venous thrombosis, or other conditions)

* Seizures

* Use or overdose of drugs-especially cocaine, amphetamines, statins, heroin, or PCP

* Trauma

* Shaking chills

* Heat intolerance and/or heatstroke

* Alcoholism (with subsequent muscle tremors)

* Low phosphate levels

Symptoms Return to top

* Abnormal urine color (dark, red, or cola colored)

* Muscle tenderness

* Weakness of the affected muscle(s)

* Generalized weakness

* Muscle stiffness or aching (myalgia)

Additional symptoms that may be associated with this disease include the following:

* Weight gain (unintentional)

* Seizures

* Joint pain

* Fatigue

Signs and tests Return to top

An examination reveals tender or damaged skeletal muscles.

* A urinalysis may reveal casts and be positive for hemoglobin without evidence of red blood cells on microscopic examination.

* A urine myoglobin test is positive.

* A serum myoglobin test is positive.

* A CPK is very high.

* A serum potassium may be very high (potassium is released from cells into the bloodstream when there is cell breakdown).

This disease may also alter the results of the following tests:

* Urine creatinine

* Serum creatinine

* CPK isoenzymes

Treatment Return to top

Early and aggressive hydration may prevent complications by rapidly eliminating the myoglobin out of the kidneys. The hydration needs with muscle necrosis may approximate the massive fluid volume needs of a severely burned patient. This may involve intravenous administration of several liters of fluid until the condition stabilizes.

Diuretic medications such as mannitol or furosemide may aid in flushing the pigment out of the kidneys. If the urine output is sufficient, bicarbonate may be given to maintain an alkaline urine state. This helps to prevent the dissociation of myoglobin into toxic compounds.

Hyperkalemia should be treated if present. Kidney failure should be treated as appropriate.

Expectations (prognosis) Return to top

The outcome varies depending on the extent of kidney damage incurred.

Complications Return to top

* Acute tubular necrosis

* Acute renal failure

Calling your health care provider Return to top

Call your health care provider if symptoms indicate rhabdomyolysis may be present.

Prevention Return to top

After any condition that may involve damage to skeletal muscle, hydration should be adequate to dilute the urine and flush the myoglobin out of the kidney.

[PRPGfirerescuetech]

For the extra credit...anyone notice similarities?

Background: Disseminated intravascular coagulation (DIC) is a complex systemic thrombohemorrhagic disorder involving the generation of intravascular fibrin and the consumption of procoagulants and platelets. The subcommittee on DIC of the International Society on Thrombosis and Hemostasis has suggested the following definition for DIC: ”An acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction”.

DIC is seen in association with a number of well-defined clinical situations, including sepsis, major trauma, and abruptio placenta, and with laboratory evidence of the following:

* Procoagulant activation

* Fibrinolytic activation

* Inhibitor consumption

* Biochemical evidence of end-organ damage or failure

DIC is a pathophysiologic term describing a continuum of events that occur in the coagulation pathway in association with a variety of disease states. DIC occurs in acute and chronic forms.

Consider DIC in patients with one of the underlying disorders listed above, with evidence of decreased or decreasing platelet counts, and with any of the laboratory findings listed above.

As the sequelae of DIC can be devastating, early clinical suspicion and laboratory diagnosis are essential. This article provides essential guidelines for the appropriate diagnosis and clinical treatment of patients with DIC.

Pathophysiology: The pathophysiology of DIC involves the initiation of coagulation via endothelial injury or tissue injury and the subsequent release of procoagulant material in the form of cytokines and tissue factors. Interleukin-6 and tumor necrosis factor may be the most influential cytokines involved in coagulation activation (via tissue factor) and may be responsible for the end-organ damage that occurs. Further, in the setting of sepsis, neutrophils and their secretory products may promote platelet-mediated fibrin formation.

Two proteolytic enzymes, thrombin and plasmin, are activated and circulate systemically. Their balance determines a bleeding or thrombotic tendency. Thrombin cleaves fibrinogen to form fibrin monomers. Thrombin ultimately potentiates the coagulation cascade and leads to small- and large-vessel thrombosis, with resultant organ ischemia and organ failure. Regulatory mechanisms of the coagulation cascade, such as tissue factor pathway inhibitor (TFPI), antithrombin III, and activated protein C, are largely defective. Plasmin, a component of the fibrinolytic system, is capable of degrading fibrin into measurable degradation products. Plasmin also activates complement. Plasmin and thrombin induce qualitative and quantitative platelet abnormalities.

Acute DIC is characterized by generalized bleeding, which ranges from petechiae to exsanguinating hemorrhage or microcirculatory and macrocirculatory thrombosis. This leads to hypoperfusion, infarction, and end-organ damage. In severe cases, patients may develop fever and a shocklike picture with tachycardia, tachypnea, and hypotension. Chronic DIC is characterized by subacute bleeding and diffuse thrombosis. Localized DIC is characterized by bleeding or thrombosis confined to a specific anatomic location. It has been associated with aortic aneurysms, giant hemangiomas, and hyperacute renal allograft rejection.

Frequency:

* In the US: Approximately 18,000 cases of DIC occurred in 1994. DIC may occur in 30-50% of patients with sepsis.

Mortality/Morbidity: Morbidity and mortality depend on both the underlying disease and the severity of coagulopathy. Assigning a numerical figure for DIC-specific morbidity and mortality is difficult. Below are examples of mortality rates in diseases complicated by DIC:

* Idiopathic purpura fulminans associated with DIC has a mortality rate of 18%.

* Septic abortion with clostridial infection and shock associated with severe DIC has a mortality rate of 50%.

* In the setting of major trauma, the presence of DIC approximately doubles the mortality rate.

Sex: Incidence is equal in males and females.

Age: No age predilection is known.

[PRPGfirerescuetech]

Acanthosis Nigricans...hows that for a rare one? Anyone? Anyone?