You are on duty in the emergency department. The nurse enters the emergency room with a male patient, aged 32, with the following vital signs: BP= 86x64mmHg, HR= 112 bpm, RR= 26irpm, Arterial oxygen saturation= 90% on ambient air, temperature = 36.2^oC. Patient is alert. You take the hand and wrist of the patient: hands are cold. Upon general inspection of the patient, only jugular stasis is noticeable. What are the most likely syndromic diagnoses for this patient?

 

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The assessment of vital signs indicates two initial syndromic diagnoses: Acute respiratory failure and Shock.

The presence of tachycardia, tachypnea, and hypoxemia indicate Acute Respiratory Failure. It is emphasized that it is not necessary to identify hypoxemia to diagnose acute respiratory failure, which is caused by the inability of the cardiorespiratory system to meet the tissue demand for oxygen. Tissue oxygenation depends on cardiac output and arterial oxygen content (which depends on hemoglobin, arterial oxygen saturation and partial pressure of oxygen).

The presence of tachycardia, tachypnea, and cold extremities, in our case associated with hypotension, suggests the diagnosis of Shock. Shock is a clinical syndrome that indicates tissue hypoperfusion; patients are usually tachycardic, tachypneic, and may have clinical signs such as decreased level of consciousness, oliguria and cutaneous hypoperfusion. Hypotension may suggest shock, but it should be noted that many patients who are in shock have normal or even higher-than-normal blood pressure.

Considering the association between shock and acute respiratory failure, we could define the following differential diagnoses:

SHOCK - DIFFERENTIAL DIAGNOSIS
SHOCK	MAIN CAUSES	PHYSIOPATHOLOGIC MECHANISM
HYPOVOLEMIC	Haemorrhage Diarrhea Cutaneous losses Reduced fluid intake	Reduced preload Reduced cardiac output
CARDIOGENIC	Myocardial infarction Valvular heart disease Arrhythmias Pulmonary edema	Reduced cardiac output Increased systemic vascular resistance
OBSTRUCTIVE	Cardiac Tamponade Hypertensive pneumothorax Pulmonary embolism	Reduced cardiac output Increased systemic vascular resistance
DISTRIBUTIVE	Sepsis Anaphylaxis Neurogenic Shock Adrenal Insufficiency	Systemic arterial vasodilation

 

The physical examination can quickly provide information that can point to one of the more likely causes of shock:

 

SHOCK - INITIAL PHYSICAL EXAMINATION
SHOCK	PHYSICAL EXAMINATION
HYPOVOLEMIC	Dehydration (dry mucous membranes and armpits) Cold extremities Reduced pulse pressure Bleeding Mucocutaneous pallor
CARDIOGENIC	Cold extremities Jugular venous distension Third heart sound (gallop) Fine crackes lung sounds
OBSTRUCTIVE	Cold extremities Cardiac tamponade: muffled heart sounds, paradoxal pulse > 10 mmHg, jugular venous distension Pneumothorax: asymmetric lung expansion, hyperressonance on percussion, tracheal deviation to the contralateral side Pulmonary embolism: jugular venous distension, lower limb edema, hepatomegaly, dullness to percussion of a second left intercostal space, accentuated second heart sound
DISTRIBUTIVE	Warm extremities Wide pulse pressure

The patient presents with cold extremities and reduced pulse pressure, pointing to a low probability of distributive shock. We should emphasize that if a patient is extremely hypovolemic, he or she can have these signs even with distributive shock. However, the patient has jugular venous distension, which reduces the possibility of hypovolemia, in turn increasing the likelihood of obstructive or cardiogenic shock. Thus associating cold extremities, jugular venous distension and vital signs (data that is obtained in a few seconds in the emergency room, highlighting the importance of patient inspection), we can establish the following syndromic diagnoses:

• ACUTE RESPIRATORY FAILURE

• SHOCK (obstructive or cardiogenic)

The following clinical evaluation should address these syndromic diagnoses in defining the etiologic diagnosis.

REFERENCES:

1. Holmes CL, Walley KR. The evaluation and management of shock. Clin Chest Med 2003 (24), 775-789.

2. Strehlow MC. Early identification of shock in critically ill patients. Emerg Med Clin N Am 2010; 28: 57-66.

 

Patient reported chest pain in the left hemithorax a day ago that worsens with breathing, and for 2 hours he has been feeling dyspnea, which started suddenly. Works as a truck driver, last month reported overwork, sometimes more than 15 hours per day. He denies previous similar episodes. On examination, patient is hydrated, cardiac auscultation is normal, there is dullness to percussion in the anterior second left intercostal space, and crackles and rhonchi were found in the right pulmonary base. Abdominal examination is normal. There is no edema of the lower limbs. Paradoxical pulse is 8 mmHg. Patient is alert and conscious.

What are the immediate measures to be taken for this patient? How do we begin our primary diagnostic investigation?

 

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As the patient is in acute respiratory failure, we must first consider two questions:

A) How do we provide oxygen?

B) Is there a need for ventilatory support?

Every patient who presents with respiratory failure must, as a first order of business, be raised to a sitting position. Oxygen must be supplied either through the catheter or a mask (open or Venturi), depending on the severity of the case. In patients with frank respiratory distress that are breathing through the mouth, a nasal oxygen catheter would have little effect, and thus the mask would be preferable. It is important to remember that we should limit the flow of oxygen to patients with chronic ventilatory respiratory failure who suffer from chronic carbon dioxide retention, such as those with chronic obstructive pulmonary disease, in order to avoid hypercapnia.

In our case, therefore, there are no chronic respiratory diseases, and we must raise the patient to the sitting position and start supplying oxygen through a mask at a rate of 5 liters per minute.

With respect to ventilatory support, remember that there are 2 types: noninvasive (CPAP / BiPAP - supplied through a face mask) and invasive (mechanical ventilation and tracheal intubation). In the case of our patient, we do not consider cardiogenic pulmonary edema or COPD exacerbation to be a cause of respiratory failure. Additionally, the patient has hypotension. Given these findings, noninvasive ventilation is not required. Patient is alert, without alteration of consciousness, with no signs of imminent cardiac arrest. Thus, this time we can provide only oxygen and seek data to obtain an etiological diagnosis.

The next immediate step is to define the cause of hypotension. Any patient in Shock should initially have his blood volume tested. Patient is hydrated with jugular stasis. Therefore, cardiogenic and obstructive shock are the main assumptions, which do not usually respond much to changes in volume. Thus, aggressive volume expansion should be delayed until the initial results of complementary tests come in.

Considering the above:

• Cardiogenic shock: the absence of alterations in cardiac auscultation (in identifiable murmurs or arrhythmias) make arrhythmia and valvular disease less likely. Acute coronary syndrome is not our first diagnostic hypothesis, because chest pain is not suggestive of ischemia (it has not radiated to the upper limbs, there is no nausea or vomiting) and the physical examination shows no signs of acute coronary syndrome (such as murmur of mitral insufficiency or gallop). In addition, the patient is young and has no risk factors for this disease.

• Obstructive shock: cardiac tamponade: tachycardia, jugular venous distension and shock may be indicative of this diagnosis, but there is no description of muffled cardiac sounds (present in 30% of patients), and the paradoxical pulse is normal (8 mmHg), which makes this diagnosis unlikely, since the paradoxical pulse will be greater than 10 mmHg in over 80% of patients with cardiac tamponade. Tension pneumothorax: no change in specific lung auscultation makes this a less probable diagnosis. Pulmonary embolism: identification of dullness in percussion in the second left intercostal space points to this diagnosis.

Based on these criteria, Pulmonary thromboembolism (PE) is our main diagnostic hypothesis.

Whenever we think of pulmonary thromboembolism, we perform the calculation of the pre-test clinical probability of pulmonary embolism. One of the most used is that of Wells, which depends on no further examination:

WELLS CRITERIA – PULMONARY EMBOLISM
CRITERIA	PONTUATION
Clinical signs of deep venous thrombosis	3
Pulmonary embolism is the most likely diagnosis	3
Tachycardia (HR > 100 bpm)	1.5
Imobilization > 3 days or surgery in last 4 weeks	1.5
Previous venous thromboembolism	1.5
Recent malignant neoplasia	1
Hemoptysis	1

 

The patient receives at least 4.5 points because, as discussed above, PE is our most likely diagnosis and the patient has HR > 100 bpm. From the point of view of clinical classification, patients with score <2 points are of low clinical probability, between 2 and 6 points are of intermediate probability and above 6 points are of high clinical probability.

In addition to classifying the clinical probability of PE, some initial complementary tests may be useful, in particular defining the differential diagnosis and assessing the risk of developing complications in actually being diagnosed with PTE.

REFERENCES

1. JAB Martinez et al. Recommendations for the management of pulmonary embolism. Bras Pneumol J 2010, 36 (Suppl 1): s1-s68.

2. Jaff MR, McMurtry MS, Archer SL. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic tromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2001, 123: 1-43.

 

The patient underwent the following tests:

Arterial blood gas analysis: pH= 7.47, pO₂= 62 mmHg, pCO₂= 22mmHg, HCO₃= 21mEq/L, BE -2; SaO₂= 89% (ambient air);

Troponin = 89 mg/dl (normal below 14 mg/dl)

CBC: Leukocytes: 9600cels/mm3, Hemoglobyn= 14.3 g/dl and Platelets= 320000cels/mm3;

Urea= 34 mg/dl; Creatinine= 0.9mg/dl

Na= 137mEq/L; K= 4.6mEq/L.

INR= 1.1.

Describe chest X-ray and electrocardiography. Interpret the arterial blood gas analysis.

Have the exams changed the initial diagnosis? What information have they given us?

How must we continue the diagnostic investigation of this patient?

 

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The patient's chest X-ray shows triangular consolidation, with the apex turned to the hilum in the lower right hemithorax and another consolidation in the left hemithorax. The consolidations are defined by the presence of air bronchograms. Remember that there are several causes of radiological consolidation, which means pathological accumulation of substances in the alveolar spaces, such as water (pulmonary edema), pus/ inflammation (pneumonia, tuberculosis), blood (alveolar hemorrhage, pulmonary infarction) or neoplasia (bronchioloalveolar adenocarcinoma or lymphoproliferative disorders).

The electrocardiogram shows the heart rate at around 108 bpm (tachycardia); tachycardia with narrow QRS complex, with regular RR interval, P wave (PR interval sinus tachycardia. Also observed was the morphology rsR' in V1 and V2 leads -> right bundle branch block.

Arterial blood gas analysis reveals hypoxemia and respiratory alkalosis.

With regards to pulmonary thromboembolism, the function of the initial complementary tests (ECG, X-ray and blood gases) aims to identify differential diagnoses; none of the three provides definitive diagnosis for pulmonary thromboembolism.

The radiographic findings may correspond to pulmonary infarction - observed image in the right hemithorax is triangular with the apex turned to the hilum (Hampton hump?).

Thus, the findings of the initial exams did not change the initial diagnosis.

Another laboratory test that brings us important information is that for troponin. In the context of pulmonary embolism, high troponin may indicate problems in the right ventricle, as already indicated by the electrocardiogram showing the right bundle branch block.

From the standpoint of diagnostic investigation, the Wells score can be used using the following strategy, according to more recent studies:

• Wells score <= 4 points: acute PTE unlikely: assessment must start with of D-dimer evaluation; if the D-dimer presents a negative value, assessment must continue; in case it presents a positive value (> 500 ng / ml), the doctor should run confirmatory tests for PE (CT angiography, radionuclide ventilation-perfusion, pulmonary angiography).

• Wells score> 4 points: acute PE: no need to collect D-dimer, the doctor should start the investigation with confirmatory tests for PE (CT angiography, radionuclide ventilation-perfusion, pulmonary angiography).

Thus, according to the clinical data presented so far, a confirmatory exam is needed for PE.

REFERENCES

1. JAB Martinez et al. Recommendations for the management of pulmonary embolism. Bras Pneumol J 2010, 36 (Suppl 1): s1-s68.

2. Jaff MR, McMurtry MS, Archer SL. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic tromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2001, 123: 1-43.

 

Patient received 500 ml of saline solution within 30 minutes. His blood pressure was 88x68 mmHg. We opted for chest CT scan:

 

Describe the findings of chest CT scan.

Could the diagnostic investigation have been done with another exam?

What is the most appropriate therapeutic approach for this patient?

 

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A chest CT scan with a mediastinal window shows numerous filling defects (thrombi) in right and left pulmonary arteries. Below, circled in red, the gaps in the right pulmonary artery; circled in yellow, the gaps in the left pulmonary artery.

We have observed numerous areas of consolidation in the lung parenchyma, predominantly in the center of the lung, bilaterally. There is a triangular area of consolidation in the right lung, which may correspond to pulmonary infarction. The areas of consolidation in the left lung may correspond to pulmonary edema (in pulmonary thromboembolism, when there is a large increase in pressure in the right chamber, there is a deviation of the interventricular septum to the left and increased filling pressures of the left ventricle; this mechanism can lead to pulmonary edema), areas of infarction or pulmonary infection (pneumonia), the latter less likely by clinical correlation.

Our patient was admitted with hemodynamic and clinical instability (hypotension, hypoxemia, respiratory failure and signs of right ventricular overload - clinical, ECG and troponin). Thus, he is a candidate for thrombolysis. Every patient diagnosed with pulmonary thromboembolism presenting with hemodynamic instability (systolic BP below 60, with no response to volume) should be considered a candidate for thrombolysis, unless contraindications exist (tables below).

Among the diagnostic methods that can be used for unstable patients are bedside echocardiography (especially transesophageal) and pulmonary angiography (angiography, through which embolectomy can be performed, is the test of choice when thrombolysis is contraindicated and the patient presents with hemodynamic instability).

PE – INDICATIONS OF THROMBOLYSIS

• Hemodinamic instability (SPB < 90 mmHg or DBP <60) • Right ventricular overload (right heart failure) in patients with no previous structural cardiac disease.

 

PE – THOMBOLYSIS CONTRAINDICATION

Previous haemorrhagic stroke Isquemic stroke in the last 6 months Neoplasia ou lesions in central nervous system Surgery or major trauma in the past 3 weeks Gastrointestinal bleeding in the last month Active bleeding

REFERENCES

1. JAB Martinez et al. Recommendations for the management of pulmonary embolism. Bras Pneumol J 2010, 36 (Suppl 1): s1-s68.

2. Jaff MR, McMurtry MS, Archer SL. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic tromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2001, 123: 1-43.

 

Patient was asked about contraindications to thrombolysis, with a negative response. He then underwent thrombolysis with rt-PA at a dose of 100 mg IV over 2 hours.

After thrombolysis treatment with low molecular weight heparin, 1 mg / kg every 12 hours was started.

Patient did not have any complications from thrombolysis, with improved blood pressure (normalization).

Mechanical ventilation was not required.

He was admitted to ICU.

On the second day of hospitalization, oral anticoagulation was started. Heparin was continued for 5 days, and removed when the INR was 2.68.

He was discharged from the hospital after 7 days.

 

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During the period from 29 November 2011 to 31 October 2012 (339 days) the 109 sixth-year medical students produced 139,634 pageviews in 4,511 accesses to our course on the Moodle platform.

Each student, on average, accessed the platform 42 times, with 1,254 pageviews.

The average daily total was 412 pageviews.

In the categories created in the form of discussion forums, students made 2,245 posts.

The categories most accessed are illustrated in the Figure below:

Although the Virtual Rounds was the most accessed category, we noted there was an increase in the number of pageviews and access on all areas in the days before exams, especially in the Quiz and Extreme Decisions categories, both of which consist mostly of multiple choice questions. The categories Radiologic Challenges, Gasometric Challenges and Bibliography showed uniform access, with no significant variation near the exam period.

Students were divided into groups of 18 students, and each group had held internships in Clinical Emergency for 2 months. Although participation in the course focused on this two-month period (63% of total accesses of all students were in the stage of Clinical Emergencies), the average number of months in which the students participated in the platform was 5.53. This indicates that even in periods outside the stage of Clinical Emergencies, students maintained interest in the platform and in the study of Clinical Emergencies.