USMLE
http://www.usmleadvice.com/keypoints.pdf

PHYSICAL EXAM
http://meded.ucsd.edu/clinicalmed/

Anatomy
http://msjensen.cehd.umn.edu/webanatomy/Default.htm
http://www.presentationgroup.com/medicallibrary/

Algorithms
http://www.medal.org/visitor/login.aspx

Health Care Guidelines
http://www.icsi.org/guidelines_and_more/index.aspx?catID=12

“Fighting for Life,” a documentary by two-time Academy Award-winning filmmaker Terry Sanders, is a portrait of American military medicine. The film tells the story of USU and shows students at the University on their journeys towards becoming military physicians and nurses.

The gripping documentary uses compelling footage, including images from the current conflicts in Iraq as well as interviews with current USU students, to illustrate U.S. Military medical personnel’s dedication to providing the best possible care for those in harm’s way both on and off the battlefield.

On January 29, 2006, Woodruff and Canadian cameraman Doug Vogt were seriously injured in an explosion from an improvised explosive device near Taji, Iraq, about 12 miles (19 km) north of Baghdad.[1] Woodruff had traveled with an ABC News team to Israel to report on the aftermath of the 2006 Palestinian elections, and then via Amman to Baghdad, so he could meet with troops before President George W. Bush’s State of the Union address for 2006.[2]

At the time of the attack, they were embedded with the U.S. 4th Infantry Division, travelling in an Iraqi MT-LB. Woodruff and Vogt were standing with their heads above a hatch, apparently filming a stand-up. Both men were wearing body armor and protective helmets at the time. Woodruff sustained shrapnel wounds; Vogt was struck by shrapnel in the head and suffered a broken shoulder. Both men underwent surgery for head injuries, with a joint Army & Air Force neurosurgical team, at the U.S. Air Force hospital south of Balad, located in Camp Anaconda, and were reported to be in stable condition.[3] Tom Brokaw reported on the Today show that Woodruff had also undergone surgery, with a portion of his skull being removed to reduce the damage from brain swelling.[4]

Woodruff and Vogt were evacuated to the United States Army Medical Command hospital at Landstuhl, Germany overnight on Sunday, January 29.[5] On ABC World News Tonight that evening, anchor Elizabeth Vargas talked about the dangers of reporting in a combat zone and wished Woodruff and Vogt well in recovery.

Wikinews has related news: Bob Woodruff injured by improvised explosive device in Iraq
After leaving Germany, Woodruff was treated for weeks at Bethesda Naval Hospital in Bethesda, Maryland. Despite the removal of part of his skull, his friend and colleague Martha Raddatz reported that he was not believed to have suffered major disfigurement.[6]

[edit] Recovery from injuries
Woodruff was kept in a medically-induced coma for several weeks to assist his recovery, and ABC News temporarily assigned Good Morning America anchors Charlie Gibson and Diane Sawyer to alternate duties on the evening newscast as co-anchor with Vargas. Vogt meanwhile was reported to be awake, mobile, and recovering.[7]

As of March 7, 2006, Woodruff’s brother reported that the ABC anchor was beginning to walk, recognize friends and family, and speak in several languages. However, he struggled with expressive aphasia for more than a year after the injury.[8] Woodruff was transferred on March 16, 2006 to a medical facility closer to his Westchester County, New York home, a sign of “continued progress in all respects,” ABC News President David Westin said in an e-mail to ABC staffers.[9] Westin’s email noted that Woodruff was able to get around, talk to and joke with his family, but that “months of further recuperation” were still required.

On April 6, 2006, ABC News released photos of Woodruff recovering at home, along with a letter thanking everyone for their support and kindness during his ongoing recovery. He especially thanked the soldiers, doctors, and nurses who had saved his life. [3]

On December 29, 2006, Woodruff’s wife, Lee, an editor at Family Fun Magazine appeared on Good Morning America to discuss family activities to celebrate the New Year. During the report, anchor Kate Snow asked Lee about her husband’s condition. Lee said that Bob was doing well and was currently filming a television documentary about his experiences. She also revealed that he had been back to Iraq since the incident to visit the soldiers with whom he was traveling at the time of his injury.

A 56-year-old obese man comes to the emergency department because of crushing chest pain that has been present for 3 hours. The pain radiates to his left arm and neck. He also complains of nausea. On physical examination, the patient is found to be sweating and his blood pressure is 164/122 mm Hg. Laboratory analysis reveals that his cardiac enzyme levels are elevated. His ECG is abnormal with ST-segment depression. Which of the following is the pathology underlying the correct diagnosis?

A. Coronary artery vasospasm caused by cigarettes and cocaine
B. Complete occlusion of the coronary arteries by a mural thrombus
C. Increased cardiac demand with coronary arteries that are greater than 75% occluded
D. Ischemic necrosis of 30% of the ventricular wall
E. Ischemic necrosis of 70% of the venricular wall

The correct answer is D. The patient has a subendocardial infarction, which is caused by ischemic necrosis of 75% occlusion of the coronary arteries by atherosclerosis. Although stable angina may produce slightly elevated cardiac enzyme levels, the clinical picture in this question is more typical of a myocardial infarction.

Answer E is not correct. Ischemic necrosis of >50% of the ventricular wall causes a transmural infarct. On ECG, there is a corresponding ST-segment elevation.

———————–

In nature, Anthrax is generally a disease found in common
livestock animals like sheep, cattle and horses.
While it has high mortality rates in infected animals of
these types, human infections are very rare. Human fatalities
are even more rare. Before the 2001 events,
the last human fatality from anthrax was in 1976.
In humans, the disease takes three forms: cutaneous,
intestinal, and pulmonary. Cutaneous anthrax involves
skin lesions which are surrounded by a ring of fl uid-fi lled
vessels. Most of these lesions resolve themselves, but
fatal infections occur in about 20% of cases.
Intestinal anthrax occurs after eating contaminated
meat. Symptoms for this type of anthrax can begin with
malaise/upset stomach, progress to severe fevers and,
in many cases, lead to shock, coma and death.
Pulmonary anthrax is caused by inhaling anthrax
spores. That’s why it is also called inhalation anthrax.
When this occurs naturally, it is usually seen in workers
who handle infected hides or fur. The onset with this
type of anthrax is slower.

First comes mild chest pain and coughing. These symptoms
can then disappear during an incubation period
that can last from a few hours to three days. This period
is followed by severe respiratory distress as the system
goes into septic shock. Before the successful treatment
of some anthrax patients with strong antibiotics,
doctors thought that pulmonary anthrax was invariably
fatal. It remains fatal around 75% of the time, depending
on how quickly antibiotics are administered..

What is leishmaniasis?
Leishmaniasis (LEASH-ma-NIGH-a-sis) is a parasitic disease that is found in parts of the tropics, subtropics, and southern Europe. It is caused by infection with Leishmania parasites, which are spread by the bite of infected sand flies. There are several different forms of leishmaniasis in people. The most common forms are cutaneous (cue-TAY-knee-us) leishmaniasis, which causes skin sores, and visceral (VIS-er-al) leishmaniasis, which affects some of the internal organs of the body (for example, spleen, liver, and bone marrow).

What are the signs and symptoms of cutaneous leishmaniasis?
People who have cutaneous leishmaniasis have one or more sores on their skin. The sores can change in size and appearance over time. They may end up looking somewhat like a volcano, with a raised edge and central crater (ulcer). Some sores are covered by a scab. The sores can be painless or painful. Some people have swollen glands near the sores (for example, under the arm if the sores are on the arm or hand).

What are the signs and symptoms of visceral leishmaniasis?
People who have visceral leishmaniasis usually have fever, weight loss, and an enlarged spleen and liver (typically, the spleen is bigger than the liver), and some abnormal blood tests. For example, patients usually have low blood counts, including a low red blood cell count (anemia), low white blood cell count, and low platelet count.

How common is leishmaniasis in the world?
The number of new cases of cutaneous leishmaniasis each year in the world is thought to be about 1.5 million. The number of new cases of visceral leishmaniasis is thought to be about 500,000.

In what parts of the world is leishmaniasis found?
In the New World (the Western Hemisphere), leishmaniasis is found in some parts of Mexico, Central America, and South America (Latin America). It is not found in Chile or Uruguay.

In the Old World (the Eastern Hemisphere), leishmaniasis is found in some parts of Asia, the Middle East, Africa, and southern Europe. It is not found in Australia or the Pacific Islands.

Overall, leishmaniasis is found in focal areas of about 88 countries. Some of these countries account for most of the world’s cases of leishmaniasis:

Over 90 percent of the cases of cutaneous leishmaniasis occur in parts of Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, and Syria (in the Old World) and in Brazil and Peru (in the New World);
Over 90 percent of the cases of visceral leishmaniasis occur in parts of India, Bangladesh, Nepal, Sudan, and Brazil.
However, the cases of leishmaniasis evaluated in the United States reflect travel and immigration patterns. For example, cases in U.S. civilian travelers typically are cases of cutaneous leishmaniasis (rather than of visceral leishmaniasis) acquired in common tourist destinations in Latin America (rather than in places in the Old World).

How do people get infected with Leishmania parasites?
The main way is through the bite of infected female phlebotomine sand flies. (Sand flies become infected by biting an infected animal or person.) People might not realize that sand flies are present because:

They do not make noise when they fly;
They are small: they are only about one-third the size of typical mosquitoes or even smaller;
Their bites might not be noticed (the bites may be painless or painful).
Sand flies usually are most active in twilight, evening, and night-time hours (from dusk to dawn). Although sand flies are less active during the hottest time of the day, they may bite if they are disturbed (for example, if a person brushes up against the trunk of a tree or other site where sand flies are resting).

Some types (species) of Leishmania parasites may also be spread by blood transfusions or contaminated needles (needle sharing). Congenital transmission (spread from a pregnant woman to her baby) has been reported.

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?

———————————————————————
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.

———————————————————————
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)

———————————————————————
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

——————————————————————–
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.

35 year old woman with calf tenderness and acute dyspnea. The arterial blood gas reveals an O2 of 76 mm hg.
Which of the following is the most common finding in PE?

A)Wheezing
B)Increased second heart sound
c)Tachypnea
d)calf swelling
e)Pulmonary rales

ANSWER C

HISTORY:
The patient is 68 year old female with a history of CHF, HTN and atrial fib who presents with a chief complaint of feeling “weak and dizzy” after ingesting a handful of her “heart pills” 3 hours prior.

PHYSICAL EXAM
General: Patient appears her stated age, with blue-tinted hair, resting quietly on a monitored bed.
Vitals: P=48 BP= 90/60 RR= 24 T= 98.6
Neck: No JVD
Lungs: Crackles at bases bilat
CV: Bradycardic, Irreg RR, no murmurs
Ext: No cyanosis, thready periph pulses
DIAGNOSTIC STUDIES
ECG: Rate of 40-50/min with 3:1 A-V block
CXR: Cardiomegaly, no acute failure
Lytes: Na=145 K=5.9 Cl=104 HCO3=24
BUN/Cr: 46/2.2
Glucose: 120

The patient hands you a brown paper bag filled with medication bottles and loose unmarked pills. Her medications include: Lanoxin 0.25; Procardia SR; Lasix m; and K-dur 20meq.

I) What is the toxicologic differential diagnosis of a patient presenting with bradycardia and hypotension?
Anticholinesterase drugs Aricept,Namenda
Digitalis
Beta blockers
Opioids Calcium channel blockers, Clonidine

II) Compare and contrast acute versus chronic digitalis toxicity

A) Acute
Typically younger patient population
Higher levels than chronic yet less symptomatic
Hyperkalemia (action on the Na+/K+ ATPase pump)
Supraventricular heart block, bradyarrythmias, general lack of ventricular arrhythmias
Levels may guide therapeutic intervention

B) Chronic
Older patients with underlying cardiac disease
Higher morbidity, mortality than acute
Greater target organ toxicity
More potential for drug interactions
Lower clinical index of suspicion, vague symptoms
Normal or hypokalemia (Pt typically on diuretics)
Arrhythmias-all types, mostly tachydysrhythmias
Digitalis levels may not guide management
Similar to other chronic toxicities (Lithium, Theophylline, Salicylates)

III) What are the indications for FAB fragments?
Severe ventricular dysrythmias
Progressive bradyarrythmias
Potassium levels >5.5
Acute postingestion levels greater than 10-15ng/ml, (levels less helpful in chronic toxicity)
Hemodynamic compromise
Concomitant renal failure
To confirm diagnosis of suspected digitalis poisoning?

Dosing of Digibind:
1) Dose(#of vials)=Serum digoxin conc(ng/ml)X Wt(kg)
______________________________
100

2) Dose(#of vials)= Total digitalis body load (mg)
____________________________
0.6mg of digitalis bound / vial

3) If amount unknown or levels unavailable:
administer 10-20 vials
IV) Adverse effects of Digibind Hypokalemia
Worsening CHF
Increased ventricular rate (rapid a fib)
Allergic Rx
IV) Is there a role for glucagon and calcium in this case?

Glucagon: first line antidote in Beta blocker overdose
May also be efficacious in CCB toxicity by increasing cAMP, activating calcium channels.
Dose: 5-10mg IVP
Calcium gluconate/calcium chloride
First line antidote in CCB overdose
Indicated for hyperkalemia/cardiovasc compromise
CONTRAINDICATED in digitalis toxicity. (Digitalis inhibits Na-K ATPase resulting in increased intracellular sodium and calcium).

CLINICAL COURSE
The patient is given 2mg of atropine with little effect. She receives a dose of activated charcoal premixed with sorbitol. The digoxin level returns with a value of 6.3ng/ml. The patient is given 10 vials of digibind FAB fragments with resolution of her hypotension and bradycardia within 30 minutes of administration. Her repeat potassium is 4.2, but repeat digoxin level is 49.0. After a 7 days in a monitored setting, she is cleared by the psychiatry service and discharged home without sequelae.

Mr. Smith, a 28 year old male presents in police custody complaining of chest pain. He has no other past medical history. No history of cardiac disease.

Patient further states that his chest pain began tonight about one hour after he was arrested by police. No history of trauma.

Social history=Smokes 1 pack/day. Occasional EtOH.

Family History= No cardiac deaths. MGM with Breast CA

Physical Exam:
Click HERE to observe the patient.
General: Patient very agitated, clutching his chest.
Vitals: P 140, BP 220/130 RR-28 Temp- 103.2F
Eyes: Pupils 7mm, equal, EOMI
Lungs: Clear Bilaterally
Heart: Regular rate and rhythm, 2+/6 systolic murmur
Abd: Soft, Non-Tender, BS+
Neuro: No focal defecits.
Skin: Diaphoretic

NEXT?

EKG Sinus Tachycardia, Large 5mm ST segment elevations in anterior leads. Unifocal PVC’s, approx 2-3/minute.

Chest X ray

Situs inversus (also called situs transversus) (aka oppositus) is a congenital condition in which the major visceral organs are reversed or mirrored from their normal positions. The normal arrangement is known as situs solitus. In other rare cases, in a condition known as situs ambiguus or heterotaxy, situs cannot be determined.

The term situs inversus is a short form of the Latin phrase “situs inversus viscerum,” meaning “inverted position of the internal organs.” Dextrocardia (the heart being located on the right side of the thorax) was first recognised by Marco Severino in 1643. However, situs inversus was first described more than a century later by Matthew Baillie.

The prevalence of situs inversus varies among different populations but is less than 1 in 10,000 people

Abd Films

The patient now admits to swallowing several “dime bags” of cocaine approximately 3 hours prior to presentation when the police raided his house.

QUESTIONS AND CONTROVERSIAL ISSUES

I) Describe the difference between a “Body packer” and “Body stuffer”

A) Body packers are drug smugglers who ingest illegal contraband methodically wrapped in multilayered condoms or latex in order to deliver the goods across international borders once safely through customs.

B) Body stuffers are those individuals who suddenly “swallow the evidence” during drug raids in carelessly wrapped single layered baggies, aluminum foil, or ziplock bags when about to be incarcerated by the authorities. Due to the faulty wrapping technique, despite less purity of the drug ingested, body stuffers are often more vulnerable to life-threatening toxicities secondary to leakage.

II) How should this patient’s cocaine-associated chest pain and hypertension be treated?

Benzodiazepines- First line therapy (in high doses)
Nitroglycerin- for control of ischemic pain and HTN
Labetalol- alpha/beta blocker (the use of propranolol will leave the alpha portion unopposed theoretically exacerbating cocaine’s toxicity).
Nitroprusside- for refractory HTN
Calcium channel blockers- controversial.

III) What would be the best mode of gastric decontamination in this setting?

Syrup of ipecac- contraindicated, patient unstable and potential for cocaine-induced seizure activity.
Gastric lavage- not very efficacious (3 hours post ingestion); low return of cocaine packets due to size of lavage tube; may rupture bags in process.
Activated charcoal- may adsorb leaking cocaine in gut
Whole bowel irrigation- (PEG solution) 1-2L/hr Rapid, efficacious, osmotically/electrolyte-safe. Clearly the choice for decontamination in this patient.

IV) Is there a role for thrombolytics in patient’s with cocaine induced myocardial ischemia?

Mechanisms of cocaine-induced myocardial ischemia
Coronary vasospasm
Accelerated atherogenesis
Thrombotic plaque formation
Consider thrombolytics if strict ECG criteria are met. However, this younger patient population will often demonstrate false positive ECG readings due to “early repolarization” and ventricular hypertrophy.
Cocaine patients are prone to intracranial bleeds, therefore, liberal use of thrombolytics is discouraged. In small case series, however, the thrombolytic complication rate is low.
At present, the use of thrombolytics in these patients remains controversial.

V) What consultations should be requested?

Cardiology- Unstable patient with acute anterior wall MI; consideration of thrombolytics.
Surgery- Patient ingested potentially lethal dose of cocaine packets, consult for emergent exploratory laparotomy to remove the source of toxicity.
Toxicology service or Poison Control Center
Radiology- Abdominal CAT scan or contrast studies
VI) Should all patients with cocaine-induced chest pain be admitted?

Overall mortality rate from cocaine-associated chest pain is low
Not all chest pain in cocaine abusers is cardiac-related (eg- PTX, pneumomediastinum, septic emboli)
Some authors recommend admitting all patients with cocaine induced chest pain to a monitored setting to R/O myocardial ischemia
Others are less conservative and send the majority of these patients home after a brief observation period.
Compromise- maintain a high index of suspicion, take a detailed cardiac history (respecting cocaine abuse as a legitimate cardiac risk factor), monitor the patient, and carefully interpret the ECG.
Patients with a known ingestion of packets of cocaine should be admitted and undergo gastric decontamination.

CLINICAL COURSE
The patient’s chest pain and hypertension eventually resolves with large doses of nitroglycerin and benzodiazepines. The patient is administered activated charcoal and polyethylene glycol solution by the ED physician. Because of the ST segment elevations, the cardiologist elects to give thrombolytics. However, since thrombolytics were “on board” the general surgeon refuses to take the patient to the OR for exploratory laparotomy and removal of the cocaine packets. The patient is transferred to the ICU, where he eventually recovers and is discharged with a 10% ejection fraction

72 year of man passed out in church
Unconscious x 5 minutes
No tonic clonic movements
Previous hx of lightheadhedness

PE
Pulse 35
BP 118/72
CV s1,s2 snl
Chest clear
LAbs wnl

What happened ?

Third degree heart block