pulmonary embolism - the great masquerader

THE SITUATION-
Acute PE, a pulmonary manifestation of a circulatory problem, is a serious condition caused by obstruction of blood flow in one or more pulmonary arteries (PA). Almost all PEs are caused by a thrombus, but they also can result from fat globules, air, amniotic fluid, septic clots, or tumor fragments.
The diagnosis of PE is correctly made in only 10% of patients over 70 years of age.In general, however, diagnosis is often missed in approximately 70% of cases and autopsy results show that up to 60% of deceased hospitalized patients have had a PE, a circumstance that has elicited to the condition the moniker the great masquerader.If left untreated, PE carries a 30% mortality rate.In patients with concurrent cardiac disease or cancer, that rate is about 20%, even with treatment of PE. However, when patients with uncomplicated PE are rapidly identified and treated appropriately, mortality rate is 2.5%.


SIGNS & SYMPTOMS-
Patients with a PE present with a variety of vague complaints, making diagnosis difficult.
The classic triad of signs and symptoms of PE (chest pain, dyspnea, and hemoptysis) are neither sensitive nor specific; they occur in fewer than 20% of patients in whom the diagnosis is made.
SIGNS-                                                    INCIDENCE-
TACHYPNEA (respiratory rate >16/min)-                 96%
CRACKLES ON CHEST AUSCULTATION-        58%
ACCENTUATED 2ND HEART SOUND-              53%
TACHYCARDIA-(heart rate >100/min)                   44%
FEVER-                                                                   43%
DIAPHORESIS-                                                     36%
S3 OR S4 GALLOP-                                              34%
THROMBOPLEBITIS SIGNS & SYMPTOMS-   32%
LOWER EXTREMITY EDEMA-                           24%
CARDIAC MURMUR-                                          23%
CYANOSIS-                                                          19%
source- www.emedicine.com/emerg/topic490.htm

PATIENT ASSESSMENT AND DIAGNOSTICS

Because of the nonspecific nature of patient complaints, clinical suspicion of PE should guide diagnostic testing.
A massive pulmonary embolism
can simulate a myocardial infarction. Chest
pain and the imminent sense of doom are main
symptoms of a massive pulmonary embolism, too. A
sinus tachycardia, hypotension, and peripheral vasocontriction
are typical signs found during physical
examination. In addition, tachypnea, distended jugular
veins, and cyanosis are often present.
In the ECG
a rotation of the frontal QRS axis to the right (resulting
in a SI/QIII type), a clockwise rotation of the horizontal
axis, and often unspecific ST−T changes are typical
signs of pulmonary embolism.
The chest radiograph
may show wedge-shaped or linear opacities of any
size or shape, a pleural effusion, or an elevated
hemidiaphragm. Blood gases show a low PaO2 and a
low PaCO2. D-dimers are elevated in the plasma
(>500 ng/L).
The diagnosis of pulmonary embolism
is most often confirmed by a spiral CT, occasionally
by lung scintigraphy, or pulmonary angiography.

CARDIOVASCULAR DIAGNOSTICS-

12-lead ECG-
There's no particular ECG abnormality found in all patients with significant PE. Obtaining a 12-lead ECG early can support a diagnosis of PE by ruling out acute myocardial infarction.
Echocardiogram-
Changes indicating increased pulmonary hemodynamics such as enlarged right-sided heart chambers, or tricuspid regurgitation may be seen. More than 75% of patients with PE have abnormalities of RV size, function, or tricuspid regurgitation.
Duplex ultrasound-
Compression ultrasonography of the lower extremities may be useful in determining the source of emboli, but it's of limited use in the emergency management of PE.

RESPIRATORY DIAGNOSTICS

Arterial blood gas (ABG) Analysis-
Nearly 90% of patients with PE are found to have hypoxemia and hypocapnia on ABG analysis.However, the absence of hypoxemia doesn't rule out the diagnosis of PE, nor is its presence specific to PE.
Chest X-ray-

The initial chest radiograph (CXR) of a patient with PE is almost always normal. With time, as surfactant is destroyed, small areas of atelectasis or an infiltrate develop. If PE is present in a large PA, this artery may be dilated proximal to the embolus with sudden constriction of the artery distally. If a pulmonary infarct has occurred, there may be tenting or a wedge-shaped infiltrate near the diaphragm and a pleural effusion. In the emergency setting, CXRs are most useful in excluding other sources of the patient's symptoms, such as pneumonia.
Ventilation-Perfusion Scan-
Nuclear VQ lung scan is the single most important diagnostic procedure for PE available to the emergency clinician. A VQ scan is indicated whenever the PE is suspected and no alternative diagnosis can be established.  The test compares the amount of perfusion in a lung segment with the degree of ventilation in that segment.  In the patient with PE, ventilation is normal but segmental perfusion is decreased or absent.
VQ scans are classified as normal, high-probability, or nondiagnostic.Nondiagnostic scans don't rule out the presence of PE.This finding demonstrates the need for a thorough medical history of the patient, clinical assessment, and maintenance of a high degree of vigilance.
Angiography-
Pulmonary arteriography is the gold standard in the diagnosis of PE.  It's indicated in patients who have a high probability of having a PE and a nondiagnostic VQ scan.When this test is performed carefully and completely, a positive pulmonary angiogram provides virtually 100% certainty that an obstruction to PA blood flow exists, whereas a negative result provides greater than 90% certainty that it does not.

OTHER LABORATORY DIAGNOSTICS

Plasma D-dimer-
This is a unique product of the breakdown of cross-linked fibrin. It can be clinically detected in a serum assay (ELISA test) that is considered positive if the level is higher than 500 ng/mL. ¹Since D-dimer isn't sensitive or specific enough to change the course of diagnostic evaluation or treatment of patients with suspected PE, the test result should be viewed as adjunctive to the clinical assessment.

 

THERAPY-

Anticoagulation,Fibrinolytics,Surgical intervention,Cardiac arrest therapy
OTHER DIAGNOSTIC LEADS-
>Patients with acute heart failure often
manifest pronounced symptoms of backward failure
(pulmonary embolism, dyspnea, and orthopnea).

>A rare symptom is hoarseness caused by compression
of the left recurrent laryngeal nerve by the dilated
pulmonary artery (Ortner syndrome).

>Chronic recurrent pulmonary embolism may lead to
pulmonary hypertension. This condition is easily differentiated
from idiopathic pulmonary hypertension by
noting the segmental defects that are demonstrated by
pulmonary scintigraphy, spiral CT, or pulmonary angiography.

Decerebrate posture/Decerebrate rigidity/Abnormal extensor reflex

 

SITE OF LESION-upper brain stem

POSTURE-the arms are adducted and extended, with the wrists pronated and the fingers flexed. The legs are stiffly extended, with plantar flexion of the feet.

In severe cases, the back is acutely arched (opisthotonos).

 

CAUSED BY-

1)VASCULAR-infarction(Brain stem), hemorrhage(Pontine,Posterior fossa)

2)MECHANICAL-tumor,abscess,any cerebral lesion that increases ICP may also produce decerebrate posture

3)METABOLIC-encephalopathy(Hepatic,Hypoglycemic,Hypoxic)

4)ACCIDENTAL-Removal of spinal fluid during a lumbar puncture to relieve high ICP may lead to cerebral compression of the brain stem

4)TRAUMA-Head trauma

URGENT-maintain airway or insert artificial airway and provide positive pressure repiration with measures to prevent aspiration as necessary.

POINTS TO NOTE-

A)Decerebrate posturing indicates the second-lowest measure of motor response, according to the GLASGOW COMA SCALE.

B)Decerbrate posture is relatively a late manifestation(i.e. preceded by other discernable signs and symptoms) in-

Brain stem tumor,Cerebral lesion,Hepatic encephalopathy,Hypoglycemic encephalopathy,etc.(i.e. in problems other than accidental and vascular)

C)Decerebrate posture sets early in Pontine hemorrhage,Posterior fossa hemorrhage,Brain stem infarction.(i.e. in vascular problems)

D)CHILDREN YOUNGER THAN 2YRS MAY NOT EXHIBT DECORTICATE POSTURE DUE TO IMMATURE CNS.BUT OFTEN IT PRESENT AS SEVERE OPISTHOTONOS AND IS USUALLY A TERMINAL SIGN AND THE MOST COMMON CAUSE BEING HEAD TRAUMA.IT CAN ALSO OCCUR IN REYE’S SYNDROME AS A RESULT OF INCREASED ICP CAUSING BRAIN STEM COMPRESSION.

HISTORY AND PHYSICAL EXAMINATION-

must include-

Vital signs,

Level of consciousness (LOC) preferably using GCS,

Pupil- size,equality, and response to light.

Deep tendon reflexes (DTRs) and

Cranial nerve reflexes, and

check for Doll's eye sign.

Next, explore the history of the patient's coma. If you're unable to obtain this information, look for clues to the causative disorder, such as hepatomegaly, cyanosis, diabetic skin changes, needle tracks, or obvious trauma. If a family member is available, find out when the patient's LOC began deteriorating. Did it occur abruptly? What did the patient complain of before he lost consciousness? Does he have a history of diabetes, liver disease, cancer, blood clots, or aneurysm? Ask about any accident or traumatic injury responsible for the coma.

INVESTIGATIONS-

Radiological-skull x-ray,CT scan,MRI,Cerebral angiography,Digital substraction angiography.

Other-EEG,Brain scan,ICP monitoring

MONITOR-neurologic status and vital signs every 30 minutes or as indicated.

Also be alert for signs of increased ICP (bradycardia, increasing systolic blood pressure, and widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature).