David Bloom, 39, NBC News Reporter in Iraq, has just died
Those of us who have been watching the hourly NBC News Reports of the Warin Iraq are shocked to learn that the main news reporter, David Bloom, has died.
What is more surprising is that it is being reported that he did not die as
a direct result of the war such as being hit by a missile or gunfire, but
because of an illness he got while covering the war.
David Bloom was embedded with US Troops as they fought their way up Iraq.
Bloom scored what many believe to be a first: broadcasting live reports as the American armored column he was traveling with fought its way north through the Iraqi desert.
Bloom was covering the war on a specially modified M-88 tank recovery
vehicle that allowed him to file live reports during the divisions campaign
from Kuwait to the outskirts of Baghdad. Bloom and his cameraman mounted agyrostabilized camera to produce jiggle-free video even when the M-88 was bumping along at 50 mph or more. An antenna transmitted the signal in real-time from its own gyrostabilized platform to an overhead satellite,which relayed it to NBC.
The 39-year-old co-anchor of the weekend “Today” show was about 25 miles south of Baghdad and packing gear early in the morning when he suddenly collapsed.He never regained consciousness and was pronounced dead.
WHAT HAPPENED? Could it have been prevented?
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DIFFERENTIAL DIAGNOSIS OF SUDDEN DEATH
1)Cardiac causes
previous hx
2)Neurological causes
previous hx
3)Pulmonary causes
previous hx
No significant hx except:
According to Business Week’s David Balfour, who was at the scene when Bloom arrived by airlift at the 703rd Battalion, 3rd Infantry Division medic station, Bloom had complained of cramping behind his knee and had sought medical advice from the United States by phone three days before he died.
The doctors suspected DVT and recommended proper medical attention. But the tenacious correspondent put duty before danger and pushed on. He took some aspirin – which can help to thwart clotting – but it was almost certainly too little too late.
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Pulmonary embolus
PE) is an extremely common and highly lethal condition that is a leading cause of death in all age groups. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. Unfortunately, the diagnosis is missed more often than it is made, because PE often causes only vague and nonspecific symptoms.
The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
[ CLOSE WINDOW ]
The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Frequency
United States
PE is the third most common cause of death in the US, with at least 650,000 cases occurring annually. It is the first or second most common cause of unexpected death in most age groups. The highest incidence of recognized PE occurs in hospitalized patients. Autopsy results show that as many as 60% of patients dying in the hospital have had a PE, but the diagnosis has been missed in about 70% of the cases. Surgical patients have long been recognized to be at special risk for DVT and PE, but the problem is not confined to surgical patients. Prospective studies show that in the absence of prophylaxis acute DVT may be demonstrated in any of the following:
General medical patients placed at bed rest for a week (10-13%)
Patients in medical intensive care units (29-33%)
Patients with pulmonary disease kept in bed for 3 or more days (20-26%)
Patients admitted to a coronary care unit after myocardial infarction (27-33%)
Patients who are asymptomatic after coronary artery bypass graft (48%)
Not only are these patient groups at high risk for clinically unrecognized DVT, but half or more of the patients with DVT also can be shown to have suffered a PE, even though the majority have had none of the classic symptoms of PE.
Mortality/Morbidity
Massive PE is one of the most common causes of unexpected death, being second only to coronary artery disease as a cause of sudden unexpected natural death at any age. Most clinicians do not appreciate the extent of the problem, because the diagnosis is unsuspected until autopsy in approximately 80% of cases.
Although PE often is fatal, prompt diagnosis and treatment can reduce the mortality rate dramatically.
Approximately 10% of patients in whom acute PE is diagnosed die within the first 60 minutes. Of the remainder, the condition eventually is diagnosed and treated in one third and remains undiagnosed in two thirds.
Among the group with PE that is correctly diagnosed and treated, only about one twelfth die from massive PE or its complications. Among the group with PE that is undiagnosed and therefore untreated, roughly one third die. The diagnosis of PE is missed more than 400,000 times in the US each year, and approximately 100,000 patients die who would have survived with the proper diagnosis and treatment.
Patients who survive an acute PE are at high risk for recurrent PE and for the development of pulmonary hypertension and chronic cor pulmonale, which occurs in up to 70% of patients and carries its own attendant mortality and morbidity.
History
Pulmonary embolism (PE) is so common and so lethal that the diagnosis should be sought actively in every patient who presents with any chest symptoms that cannot be proven to have another cause.
Symptoms that should provoke a suspicion of PE must include chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, hemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax.
The classic triad of signs and symptoms of PE (hemoptysis, dyspnea, chest pain) are neither sensitive nor specific. They occur in fewer than 20% of patients in whom the diagnosis of PE is made, and most patients with those symptoms are found to have some etiology other than PE to account for them. Of patients who go on to die from massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have hemoptysis. Nonetheless, the presence of any of these classic signs and symptoms is an indication for a complete diagnostic evaluation.
Many patients with PE are initially completely asymptomatic, and most of those who do have symptoms have an atypical presentation.
Patients with PE often present with primary or isolated complaints of seizure, syncope, abdominal pain, high fever, productive cough, new onset of reactive airway disease (“adult-onset asthma”), or hiccoughs. They may present with new-onset atrial fibrillation, disseminated intravascular coagulation, or any of a host of other signs and symptoms.
Pleuritic or respirophasic chest pain is a particularly worrisome symptom. PE has been diagnosed in 21% of young, active patients who come to the ED complaining only of pleuritic chest pain. These patients usually lack any other classical signs, symptoms, or known risk factors for pulmonary thromboembolism. Such patients often are dismissed inappropriately with an inadequate workup and a nonspecific diagnosis, such as musculoskeletal chest pain or pleurisy.
Physical
Massive PE causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal. Initially, abnormal physical findings are absent in most patients with PE.
After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by x-ray.
New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard.
The spontaneous onset of chest wall tenderness without a good history of trauma is always worrisome, because patients with PE may have chest wall tenderness as the only physical finding.
In patients with recognized massive PE, the incidence of physical signs has been reported as follows:
96% have tachypnea (respiratory rate >16/min)
58% develop rales
53% have an accentuated second heart sound
44% have tachycardia (heart rate >100/min)
43% have fever (temperature >37.8°C)
36% have diaphoresis
34% have an S 3 or S 4 gallop
32% have clinical signs and symptoms suggesting thrombophlebitis
24% have lower extremity edema
23% have a cardiac murmur
19% have cyanosis
Causes
Hypercoagulable states
Prolonged venous stasis or significant injury to the veins can provoke DVT and PE in any person, but increasing evidence suggests that spontaneous DVT and PE nearly always are related to some underlying hypercoagulable state. Other identified “causes” most likely serve only as triggers for a system that is already out of balance.
Hypercoagulable states may be acquired or congenital. An inborn resistance to activated protein C is the most common congenital risk factor for DVT that has been identified to date. Most patients with this syndrome have a genetic mutation in factor V known as “factor V Leyden,” although other mechanisms also can produce a resistance to activated protein C.
Primary or acquired deficiencies in protein C, protein S, or antithrombin III are also common underlying causes of DVT and PE.
Risk markers: The most important clinically identifiable risk markers for DVT and PE are a prior history of DVT or PE, recent surgery or pregnancy, prolonged immobilization, or underlying malignancy. Many other recognized markers of risk for venous thromboembolic disease are listed here.
AIDS (lupus anticoagulant)
Antithrombin III deficiency
Behçet disease
Blood type A
Burns
Catheters (indwelling venous infusion catheters)
Chemotherapy
Congestive heart failure (CHF)
Drug abuse (intravenous [IV] drugs)
Drug-induced lupus anticoagulant
DVT in the past
Estrogen replacements (high dose only)
Fibrinogen abnormality
Fractures
Hemolytic anemias
Heparin-associated thrombocytopenia
Homocysteinemia
Homocystinuria
Hyperlipidemias
Immobilization
Malignancy
Myocardial infarction
Obesity
Old age
Oral contraceptives
PE in the past
Phenothiazines
Plasminogen abnormality
Plasminogen activator abnormality
Polycythemia
Postoperative
Postpartum period
Pregnancy
Protein C deficiency
Protein S deficiency
Resistance to activated protein C
Systemic lupus erythematosus
Thrombocytosis
Trauma
Ulcerative colitis
Varicose veins
Venography
Venous pacemakers
Venous stasis
Warfarin (first few days of therapy)
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Differential Diagnoses
Acute Coronary Syndrome
Pneumonia, Bacterial
Acute Respiratory Distress Syndrome
Pneumonia, Immunocompromised
Altitude Illness – Pulmonary Syndromes
Pneumonia, Mycoplasma
Anemia, Acute
Pneumonia, Viral
Aortic Stenosis
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Asthma
Pneumothorax, Tension and Traumatic
Atrial Fibrillation
Pulmonary Embolism
Cardiomyopathy, Dilated
Pulmonic Valvular Stenosis
Cardiomyopathy, Restrictive
Respiratory Distress Syndrome, Adult
Chronic Obstructive Pulmonary Disease and Emphysema
Shock, Cardiogenic
Congestive Heart Failure and Pulmonary Edema
Shock, Septic
Hantavirus Cardiopulmonary Syndrome
Superior Vena Cava Syndrome
Mitral Stenosis
Syncope
Myocardial Infarction
Toxic Shock Syndrome
Myocarditis
Pericarditis and Cardiac Tamponade
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LAB TEST
D-dimer is a unique degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin. D-dimer is measured by latex agglutination or by an enzyme-linked immunosorbent assay (ELISA) test that is considered positive if the level is greater than 500 ng/mL.
At the present time, D-dimer alone is not sensitive or specific enough to rule out or rule in the diagnosis of PE. Its adoption in many emergency departments has increased the number of patients undergoing some evaluation for PE but has not led to any significant change in the frequency with which the diagnosis is confirmed. A patient with signs or symptoms suggestive of DVT and PE may have a positive or a negative D-dimer and still may have a final diagnosis discordant with the D-dimer and/or discordant with the clinical impression. Although recent data suggest that strongly elevated D-dimer may substantially increase the risk for PE, whether or not this translates into more intensive investigations or treatments is yet to be studied.
Imaging Studies
The initial chest x-ray (CXR) findings of a patient with PE are virtually always normal, although on rare occasions they may show the Westermark sign (ie, a dilatation of the pulmonary vessels proximal to an embolism along with collapse of distal vessels, sometimes with a sharp cutoff).
Over time, an initially normal CXR often begins to show atelectasis, which may progress to cause a small pleural effusion and an elevated hemidiaphragm.
After 24-72 hours, one third of patients with proven PE develop focal infiltrates that are indistinguishable from an infectious pneumonia.
A rare late finding of pulmonary infarction is the Hampton hump, a triangular or rounded pleural-based infiltrate with the apex pointed toward the hilum, frequently located adjacent to the diaphragm.
Because CXR is unreliable, conduct high-resolution multidetector computed tomographic angiography (MDCTA) in patients suspected of having PE.
MDCTA has been shown to have sensitivity and specificity comparable to that of contrast pulmonary angiography, and, in recent years, has become accepted both as the preferred primary diagnostic modality and as the criterion standard for making or excluding the diagnosis of pulmonary embolism.
In many patients, multidetector CT scans with intravenous contrast can resolve third-order pulmonary vessels without the need for invasive pulmonary artery catheters.
MDCTA is more likely to miss lesions in a patient with pleuritic chest pain due to multiple small emboli that have lodged in distal vessels, but these lesions also may be difficult to detect using conventional angiography.
The overall negative predictive value of MDCTA for pulmonary embolism is greater than 99%.
New 3-dimensional rendering displays promise to improve the performance of these high-resolution scans even more.
Electrocardiography
The most common ECG abnormalities in the setting of PE are tachycardia and nonspecific ST-T wave abnormalities. The finding of S1-Q3-T3 is nonspecific and insensitive in the absence of clinical suspicion for PE.
Any other ECG abnormality may appear with equal likelihood, but none are sensitive or specific for PE.
The classic findings of right heart strain and acute cor pulmonale are tall, peaked P waves in lead II (P pulmonale), right axis deviation, right bundle-branch block, an S1-Q3-T3 pattern, or atrial fibrillation. Unfortunately, only 20% of patients with proven PE have any of these classic ECG abnormalities.
If ECG abnormalities are present, they may be suggestive of PE, but the absence of ECG abnormalities has no significant predictive value.
One fourth of patients with proven PE have ECGs that are unchanged from their baseline state.
Emergency Department Care
Fibrinolytic therapy has been the standard of care for patients with massive or unstable PE since the 1970s. Unless overwhelming contraindications are evident, a rapidly acting fibrinolytic agent should be administered immediately to every patient who has suffered hypotension (even if resolved) or is significantly hypoxemic from PE.
Improvement of hypotension in response to hydration or pressors does not remove the indication for immediate fibrinolysis. The fact that hypotension has occurred at all is a sufficient indication that the patient has exhausted his or her cardiopulmonary reserves and is at high risk for sudden collapse and death.
Fibrinolysis also is indicated for patients with PE who have any evidence of right heart strain, because evidence indicates that the mortality rate can be cut in half by early fibrinolysis in this patient population.
Today, fibrinolysis may be considered for any patient with PE who lack specific contraindications to the therapy. Some centers now regard fibrinolysis as the primary treatment of choice for all patients with PE. Interventional radiology has made it possible to perform transcatheter fibrinolysis for patients who have DVT without evidence of PE. Over the past 20 years, a large number of small studies and a small number of large studies have demonstrated that fibrinolytic therapy reduces the mortality rate, morbidity, and rate of recurrence of PE regardless of the size or type of PE at the time of presentation.
Heparin reduces the mortality rate of PE because it slows or prevents clot progression and reduces the risk of further embolism.
Heparin does nothing to dissolve clot that has developed already, but it is still the single most important treatment that can be provided, because the greatest contribution to the mortality rate is the ongoing embolization of new thrombi. Prompt effective anticoagulation has been shown to reduce the overall mortality rate from 30% to less than 10%.
Early heparin anticoagulation is so essential that heparin should be started as soon as the diagnosis of pulmonary thromboembolism is considered seriously. Anticoagulation should not wait for the results of diagnostic tests: if anticoagulation is delayed, venous thrombosis and PE may progress rapidly.
Oxygen should be administered to every patient with suspected PE, even when the arterial PO2 is perfectly normal, because increased alveolar oxygen may help to promote pulmonary vascular dilatation.
IV fluids may help or may hurt the patient who is hypotensive from PE depending on which point on the Starling curve describes the patient’s condition.
A Swan-Ganz catheter is helpful to determine whether a fluid bolus is indicated; as an alternative, a cautious trial of a small fluid bolus may be attempted, with careful surveillance of the systolic and diastolic blood pressures and immediate cessation if the situation worsens after the fluid bolus.
Improvement or normalization of blood pressure after fluid loading does not mean the patient has become hemodynamically stable.
Fibrinolysis is indicated for any patient with a PE large enough to cause hypotension, even if the hypotension is transient or correctable. As noted above, early fibrinolysis may reduce the mortality rate by 50% for patients who have right ventricular dysfunction due to PE, even if they are hemodynamically stable.
Cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS) protocols are of no value in patients whose cardiac arrest is due to PE, since obstruction of the pulmonary circuit prevents oxygenated blood from reaching the peripheral and cerebral circulation.
The only management approaches likely to be helpful in this situation are emergency cardiopulmonary bypass or emergency thoracotomy.
If cardiopulmonary bypass with extracorporeal membrane oxygenation is available, it may be lifesaving for patients with massive PE in whom cardiac arrest has occurred or appears imminent.
Prior to the introduction of emergency cardiopulmonary bypass, the expected mortality rate after cardiac arrest from PE was 100%. Although experience with the technique is limited, one study reported the complete recovery of 7 of 9 patients when cardiopulmonary bypass was used to stabilize the patients for operative embolectomy.
If emergency cardiopulmonary bypass is not available, several case reports suggest that immediate bilateral thoracotomy and massage of the pulmonary vessels may dislodge a saddle embolus and restore circulation to part of the pulmonary vascular tree.
This aggressive procedure is appropriate in patients with cardiac arrest from proven or highly likely PE, because the expected mortality rate without the procedure is 100%.
The procedure is not one to be used as a “last resort” after all other efforts fail. Thoracotomy must be carried out immediately to be of any value, because in cardiac arrest from PE, closed-chest CPR is not able to provide any blood flow to the cerebral circulation.
Compression stockings
Compression stockings that provide a 30-40 mm Hg compression gradient should be used, because they are a safe and effective adjunctive treatment that can limit or prevent extension of thrombus.
True gradient compression stockings (30-40 mm Hg or higher) are highly elastic, providing a gradient of compression that is highest at the toes and gradually decreases to the level of the thigh. This reduces capacitive venous volume by approximately 70% and increases the measured velocity of blood flow in the deep veins by a factor of 5 or more. Compression stockings of this type have been proven effective in the prophylaxis of thromboembolism and are also effective in preventing progression of thrombus in patients who already have DVT and PE.
A 1994 meta-analysis calculated a DVT risk odds ratio of 0.28 for gradient compression stockings (as compared to no prophylaxis) in patients undergoing abdominal surgery, gynecologic surgery, or neurosurgery.
Other studies have found that gradient compression stockings and low-molecular-weight heparin (LMWH) were the most effective modalities in reducing the incidence of DVT after hip surgery; they were more effective than subcutaneous unfractionated heparin, oral warfarin, dextran, or aspirin.
The ubiquitous white stockings known as “anti-embolic stockings” or “Ted hose” produce a maximum compression of 18 mm Hg. Ted hose rarely are fitted in such a way as to provide even that inadequate gradient compression. Because they provide such limited compression, they have no efficacy in the treatment of DVT and PE, nor have they been proven effective as prophylaxis against a recurrence.
True 30-40 mm Hg gradient compression pantyhose are available in sizes for pregnant women. They are recommended by many specialists for all pregnant women because they not only prevent DVT, but they also reduce or prevent the development of varicose veins during pregnancy.
