1. Given the pt’s history and physical exam list your differential diagnosis including at least 5 possible diagnoses. (Remember the differential diagnosis should be broad and really just include causes that could account for the relevant symptoms) Essentially what could account for acute onset dyspnea, chest pain, and tachypnea.
Deep vein thrombosis (DVT)
Pulmonary embolism
Pnemonia
Myocardial Infaction (MI)
Asthma attack
Chronic obstructive pulmonary disease (COPD)
Hemothorax
Pneomothorax
2. Now given the clinical presentation, physical exam and labs what is your top diagnosis? (Use your differential and think through what data lead you to believe your top diagnosis is correct and go against the others)
The acute onset of symptoms makes COPD unlikely because the patient has not previously exhibited symptoms of COPD. Although the patient does have asthma, albuterol did not alleviate her symptoms, indicating that it most likely was not an asthma attack. The normal EKG (no ST wave elevation/depression etc) plus normal troponin (<0.01 ng/mL; it would be high if myocardiocytes were ischemic and rupturing) indicate that it is probably not an MI. Further, the patient denies radiating chest pain, nausea, and vomiting. Also, she is only 35 years old, which further contradicts normal presentation of MI. The radiological interpretation of the chest X-ray largely rules out hemothorax and pneumothorax. Pneumonia seems possible, especially given that the patient is exhibiting signs of an upper respiratory tract infection. However, the patient was afebrile before the onset of acute symptoms (the current slight fever is likely due the trauma and stress). Further, the procalcitonin levels are normal (<0.05mcg/L), but would have been elevated in the case of infection (i.e. pneumonia), especially bacterial. Her white blood cell count is slightly elevated (12,000 cells/ mL vs normal range of 3500-1000 cells/mL), but is likely due to her upper respiratory tract infection, and likely would be much higher in the case of pneumonia.
A pulmonary embolism, secondary to a DVT, seems most likely. The onset of symptoms was preceded by 14 hours without movement. Edema in her left leg was noted; asymmetric edema is indicative of a DVT in the affected leg. The patient is taking oral contraceptives which is associated with DVT. Further elevated D-dimer (a byproduct of fibrinolysis) levels (2000 ng/mL vs normal: <250 ng/mL), are indicative of a large blood coagulation event. All of this in combination with a history of DVT, points to DVT.
The chest pain, dyspnea, hymoptasis, tachypnea, wheezing breath sounds, in combination with the evidence for DVT, strongly point to a pulmonary embolism secondary to a DVT.
3. Given your top diagnosis what specific tests do you need to run in order to confirm it?
The Wells score is an algorthim used to predict the likelyhood of a pulmonary embolism based on the symtoms with which the patient presents. Points are added to a patient's score based on those symtoms. The algorithm is as follows:
clinically suspected DVT — 3.0 points
alternative diagnosis is less likely than PE — 3.0 points
tachycardia (heart rate > 100) — 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
history of DVT or PE — 1.5 points
hemoptysis — 1.0 points
malignancy (with treatment within six months) or palliative — 1.0 points
Interpretation:
Score >6.0 — High (probability 59% based on pooled data)
Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data)
Score <2.0 — Low (probability 15% based on pooled data)
Based on the patient's presentation with tachycardia, hemotysis, and clinicaically suspected DVT, she has a Well's score of 7; thus, a high probability of PE. An imaging study should be performed to confrim.
A pulmonary angiogram could be used to highlight any obstructions in the pulmonary vasculature, but is relatively invasive and only provides information about pulmonary circulation. A more recommended test would be CT, which could locate thrombosis both in the leg (to diagnose DVT) and the lung (to diagnose pulmonary embolism).
4. Results of a VQ Scan are shown below. Before interpreting the results below please elaborate on the following:
a.What is the ventilation perfusion ratio (V/Q ratio)? (Include a short discussion on hypoxic vasoconstriction)
The ventilation perfusion ratio quantifies the relative rates of air and blood flow in the lungs. The normal ventilation perfusion ratio about 0.84 L of air/ L blood. This normal ratio ensures that there is not a “waste” of blood flow or a “waste” of air flow.
The lung parenchyma is unique in that in response to hypoxia it vasocontricts (most other tissues vasodilate to increase blood and secondarily oxygen flow) in order to maintain a normal ventilation to perfusion ratio. This maintains the high efficiency of gas exhange around a normal V/Q ratio thus will not "waste" energy with uncessarily high blood flow.
b.What is a V/Q defect? Does a regional V/Q mismatch normally exist in the lungs? What does it tell you? What do you expect for this situation? (Include short discussion of west zones)
V/Q defect is a deviation from the normal V/Q ratio. When V/Q is much less than 0.84, blood is perfusing unventilated alveoli gas exchange is considered “ventilation limited” (this phenomenon is called “shunting”). When V/Q is very large, that indicates that blood flow is much lower than airflow or “perfusion limited"). Because an upright individual’s lungs are subject to a gravitational field the ventilation and perfusion vary depending on the relative location of the tissue within the lung. In the apex of the lung the vascular pressure is lower than the alveolar pressure resulting in slight collapse of the capillaries, in increase in vascular resistance, and decrease in blood flow. Thus at the apex of the lung V/Q is about 3.3. At the base of the lung the opposite is true. The vascular pressure is much high than the alveolar pressure, resulting in distended capillaries, decreased resistance and increased blood flow. Further the distended capillaries partially block the air space. Thus V/Q is about 0.6.
The lungs are divided into 4 zones depending on the relationship between pulmonary arterial pressure (P_PA), pulmonary venous pressure (P_PV) and alveolar pressure (P_A). Zone 1: P_A > P_PA > P_PV. Zone 2: P_PA > P_A > P_PV. Zone 3 & 4: P_PA > P_PV > P_A. Additionally in zone 4 the interstitial pressure is high enough to partially collapse the extra-alveolar vessels.
Pathologies can lead to V/Q mismatching as well, including pulmonary embolism. Becuase there exists a blockage in the blood the effected areas of the lung these areas will experience a higher V/Q ratio than they normally would. This reduces the effienency of gas exhange because there is much more air being ventilated than blood for it to exhange gas with.
c.What is a V/Q scan? How is it performed?
A V/Q scan is test to qualitatively image the spatial relationship between ventilation and perfusion. The patient inhales a radio isotope gas and positron emission tomography (PET) is used to visual ventilation in the lungs. The absence of radio isotope in a portion of the lungs indicates poor ventilation. Then a radio isotope is injected into the vasculature again PET is used to visualize the distribution of the isotope within the pulmonary vasculature (the absence of radio isotope in a portion of the lungs indicates poor perfusion). Comparison between these two images allows a physician to understand the V/Q relationship.
d.How would O2 help this patient and how would it change the V/Q ratio?
The patient has imparied purfusion of alveoli due to the embolism, which results a higher V/Q ratio. Providing gas with a higher oxygen concentration would improve the efficiency of gas exchange but not improve ventilation. Although ventilation (total air flow) would remain the same, the concentration of oxygen within the air would be increased allowing for more efficient oxygen uptake into the blood. Beyond this, the pulmonary vasculature would vasodilate in the presence of increased oxygen concentration. This will decrease pulmonary vascular resistance and increase blood flow, thus decreasing the V/Q ratio.
A V/Q mismatch results in redecues the efficiency of gas exchange, thus the gradient of blood gas partial pressures will increase from the arterial blood and the alveoli (A-a gradient). Specifically the average partial pressure of CO2 will increase in the arterial blood and drecrease in the alveoli relative to normal. Further O2 partial pressures in the arterial blood will decrease and alveolar increase. Administartion of supplemental O2 will increase the efficiency of diffusion by increasing the O2 partial pressure gradient across air blood barrier (i.e. V = D_f *(P_a - P_A)). This will improve the patients comprimised oxygen uptake.
Administration of
e.What is the interpretation of the scan below (Fig 1)? Match this up with the clinical findings.
There is almost no perfusion to the entire left lung as compared to the right lung (seen in the posterior image). There is a slight decrease in ventilation in the left lung (as compared to the right), probably secondary to the decreased purfusion. This points to a pulmonary embolism in her left lung very close the hilum of the left lung. This is consistent with the wheezing sounds ascultated in the base of the left lung and normal breath sounds in the right lung.
5. Given the positive diagnosis and confirmation of your suspicions what additional tests might be indicated in this patient. Why is that important (Hint: Where did the embolus come from? There was a clinical finding and a major criteria of well’s score that would indicate further testing)
The Well's score criteria of tachycardia, hemoptysis, and previous DVT strongly indicate the source of the pulmonary embolism was a DVT in the leg. An ultrasound could be performed on the leg to confirm that the source of the embolus was the leg. An ultrasound would be capable of visualizing blood flow within the leg and highlight an embolus
6. What do we do now that we have the diagnosis? What is the mainstay treatment for a PE? Does this actually remove the clot? There are newer treatment modalities available what is the evidence for these? (Hint: Einstein PE trial)
Thrombolytics, a thrombus disolving agent, can be given in the case the the PE is life threatening. A commonly used thrombolytic in this case, is tissue plasminogen factor. This type of therapy dissolves an existing fibrin meshwork or thrombus. More commonly though blood thinners (i.e. anticoagulants) such as warfarin or heparin are given. This type of treatment prevent clot growth but does not remove the clot. Warfarin prevents the formation of clotting factors II, VII, IX and X, whereas heparin indirectly inactivates thrombin. Heparin is for acute treatment and Warfarin is a long term treatment over the course of several months. A new shorter term treatment is rivaroxaban which is a direct factor Xa inhibitor. It has been shown to be effective as existing acute heparin therapy.