cases

[kasrainia]

BACKGROUND
A 65-year-old man presents to the emergency department complaining of difficulty breathing. He describes worsening dyspnea on exertion, which is often associated with chest tightness, wheezing, and coughing. The patient's dyspnea has worsened so that he can hardly walk from his couch to the bathroom without becoming extremely short of breath. He had been getting over a cold, with several days of nasal congestion, clear rhinorrhea, and nonproductive cough. He reports having been healthy his whole life and has not been to see a physician in at least 2 decades. However, on the review of symptoms, the patient mentions that he has gradually curtailed his activities, such as gardening, shoveling snow, and even walking in the mall, because he is increasingly "getting winded." He smokes 2 packs of cigarettes daily, a habit he has be been trying to break for at least 30 years.

On examination, the patient is alert but appears to be in respiratory distress, with mild retractions and pursed-lipped breathing. He is afebrile. His blood pressure is 140/85 mm Hg, and his pulse rate is 103 beats per minute and mostly regular. His respiratory rate is 22 breaths per minute, and pulse oximetry shows a reading of 91% on room air. His breath sounds are diminished throughout, with a markedly prolonged expiratory phase and faint expiratory wheezes in the upper lung fields. Cardiac examination reveals distant heart sounds with a somewhat prominent P2. He has no murmur, gallop, or pericardial rub. His skin is cool and dry. He has trace edema at his ankles but no cyanosis or clubbing. Electrocardiography (ECG) is performed (see Image).

What is the diagnosis?
Hint
The ECG results suggest a chronic condition.

[Nabilsabri]

chronic obstructive pulomnary condition.

Where is the mentioned ECG?

[kasrainia]

sorry the ECG didn't appear go to this link to visualize it
http://master.emedicine.com/email/ecg/ecg26/ecg26answer.html

:smiley20:
wright answer

Answer
Chronic obstructive pulmonary disease (COPD): This ECG demonstrates a constellation of findings that suggests COPD, namely, sinus tachycardia, a vertical or rightward axis, P pulmonale, low QRS voltage (particularly in the limb leads), and an incomplete right bundle branch block (RBBB).

COPD is generally not diagnosed on the basis of ECG findings. However, the signs and symptoms of cardiac and pulmonary disease overlap substantially (Marantz, 1990). It is not unusual for ECG to be the first diagnostic test performed in patients with long-standing COPD. Knowledge of the usual ECG manifestations of COPD enables the clinician to recognize uncharacteristic abnormalities, which often represent the effects of superimposed illnesses or drug toxicity (Rodman, 1990).

Tachycardia is common in individuals with exacerbations of COPD, occurring as a compensatory mechanism for low oxygen delivery (in the setting of hypoxia) or poor right ventricular function (in the setting of cor pulmonale). Sinus tachycardia is most common, but other supraventricular arrhythmias, such as atrial tachycardia (unifocal or multifocal), atrial fibrillation, and atrial flutter, can also be seen (McCord, 1998; Gorecka, 1997).

P pulmonale (ie, a P wave amplitude of >2.5 mm) is a frequently reported but relatively insensitive predictor of right atrial enlargement (Kaplan, 1994). In patients with COPD, the amplitude of the P wave is in fact dynamic and tends to be more prominent during an acute exacerbation than at other times (Asad, 2003).

A vertical or rightward axis is another manifestation of pulmonary hypertension (Bossone, 2003). Similarly, complete or incomplete RBBB and/or right ventricular hypertrophy are common in patients with cor pulmonale.

Low voltage, particularly in the limb leads, is another ECG characteristic of patients with COPD. This finding is classically attributed to increased impedance through a hyperinflated chest. However, low voltage is not directly correlated with hyperinflation, and it is neither sensitive nor specific for COPD (Sorbello, 1982).

For more information on COPD, see the eMedicine articles Chronic Obstructive Pulmonary Disease (within the Internal Medicine specialty) and Chronic Obstructive Pulmonary Disease and Emphysema (within the Emergency Medicine specialty).

[Nabilsabri]

Telephone triage in dyspnea in an adult patient
1- Ask the next 3 question: Sever dyspnea, New dyspnea at rest and/or Sudden onset of chest pain??


If the answer is yes, Tell go to emergency department.


If the answer is no, There are two possibilities

upon brief history:

A. History of CHF or progressive dyspnea >>> Inform home physician increase diuretic, weigh daily, advice office visit or emergency department when indicated and do home health visit.
B. History of COPD or Asthma >>> Inform home physician adjust bronchodilator dose, add corticosteroids, consider antibiotics, advice office visit or emergency department when indicated and do home health visit.

Clues to diagnose dyspnea:
dyspnea


+ Cough >>> Asthma or pneumonia.
+ sever sore throat >>> Epiglottitis
+ Pleuritic chest pain >> pericarditis, Pulmonary embolism, Pneumothorax or pneumonia
+ Orthopnea or paroxysmal nocturnal dyspnea or edema>> CHF
+ Tobacco use>> COPD, CHF, Pulmonary embolism
+ indigestion and dysphagia >> GORD and Aspiration
+ Barking cough >> Croup infections.

[القصرعينية]

<TABLE cellSpacing=0 cellPadding=8 width="100%"><TBODY><TR><TD colSpan=3>BACKGROUND
A previously healthy 22-year-old woman presents to the emergency department with acute shortness of breath. Her shortness of breath had become worse with exertion and was associated with pleuritic chest pain for 2 days. She has had a fever, nonproductive cough, nausea, vomiting, and arthralgia.

On presentation, she is febrile with a temperature 38.6°C, blood pressure 88/54 mm Hg, pulse of 104 bpm, respiratory rate of 28 breaths per minute, and oxygen saturation of 88% on room air; this last finding improved to 92% with the supplemental oxygen given at 2 L/min. She was in moderate respiratory distress; however, she can speak in full sentences. Physical examination reveals absent breath sounds throughout the right thorax, with decreased breath sounds halfway up the left thorax. Other findings are associated egophony, decreased fremitus, and dullness to percussion on the right thorax. She has no jugular venous distension, edema on her lower extremity, or rash.

What is the diagnosis?</TD></TR><TR><TD colSpan=3>Hint
The pleural fluid was positive for lupus anticoagulant, anticardiolipin antibodies, anti–double-stranded DNA (1:40), and antinuclear antibodies (1:10,000). </TD></TR></TBODY></TABLE>

[Nabilsabri]

Sounds to be pleural effusion and God knows.

[مصباح]

the level of the ct is not known !!!

some strange findings :

although the right ling is collapsed, and there ia massive effusion ....
the trachea lies perfectly in place !!!
but cardiac shadow is markedly pushed to the left

[Nabilsabri]

The level of CT is thorax of a human being

[القصرعينية]

the level is expected from the x-ray i think
let me figure this out:
minimal effusion= no shift of mediastinum
moderate amount= shift of the apex alone to opposite side
massive effusion =shift of both apex & trachea


Answer
Lupus pneumonitis: The chest radiograph reveals a small pleural effusion on the left side, one fourth of the way up, in addition to the right-sided pleural effusion three fourths of the way up, with mediastinal shift to the left. The patient was admitted to the intensive care unit because of acute respiratory distress. Contrast-enhanced chest CT confirmed the right-sided pleural effusion, small left-sided effusion, and pulmonary infiltrates.

Thoracentesis was performed, and samples were negative for infection on cultures and Gram staining. In addition, cytology was noted to be unremarkable for malignant or atypical cells. Lactate dehydrogenase (LDH) was greater than 200 U, with a fluid-to-blood ratio of 0.75. Protein levels were increased as well, with a fluid-to-blood ratio of 0.6. The patient was found to have an exudative process. (In 1972, Light and colleagues described criteria for differentiating a transudate from an exudate: if LDH is more than 200 U, the fluid-to-blood LDH ratio is more than 0.6, or the fluid-to-blood protein ratio is more than 0.5, there is a 99% positive predictive value for an exudate with a corresponding 98% negative predictive value.) Additionally, as previously noted, the pleural fluid was positive for lupus anticoagulant, anticardiolipin antibodies, anti–double-stranded DNA (1:40), and antinuclear antibodies (1:10,000).

Given the results of the patient's pleural fluid analysis, systemic lupus erythematosus (SLE) presenting with acute pneumonitis was diagnosed. The patient's condition improved with intravenous solumedrol, and she was discharged home several days later with a prescription for oral prednisone. SLE is a chronic multisystemic microvascular inflammatory disease. In the United States, the incidence of SLE is 1 case per 2000 population, with an increased prevalence in women of childbearing age and in certain ethnic groups (eg, African Americans, some Polynesian groups).

Pulmonary manifestations of SLE include both acute and chronic processes. Acute complications include pulmonary embolus, pneumonia, diffuse alveolar hemorrhage, and lupus pneumonitis. The diagnosis in this case, acute lupus pneumonitis, is an uncommon presentation that accounts for as many as 10% of all cases of lupus. The symptoms of lupus pneumonitis are severe dyspnea, tachypnea, fever, pleurisy, cough, basilar rales, and hypoxia. Patients have no apparent infection. Radiographs show atelectasis and infiltrates predominantly in the lower lobes. In addition, up to 30% of patients have pleural effusion. Pathologically, findings of diffuse alveolar damage are seen in patients with lupus pneumonitis.

Lupus pneumonitis usually responds to glucocorticoids. Intravenous pulse steroid therapy or immunosuppressive drugs may be considered if patients do not improve in 3 days. Lupus pneumonitis may progress to pulmonary fibrosis and, eventually, pulmonary hypertension. Untreated, the prognosis of patients with lupus pneumonitis is poor, with short-term mortality rates approaching 50%.

For more information on lupus pneumonitis, see the eMedicine articles Systemic Lupus Erythematosus (http://www.emedicine.com/med/topic2228.htm) (within the Internal Medicine specialty), Systemic Lupus Erythematosus (http://www.emedicine.com/emerg/topic564.htm) (within the Emergency Medicine specialty), and Systemic Lupus Erythematosus (http://www.emedicine.com/pmr/topic135.htm) (within the Physical Medicine and Rehabilitation specialty).

[القصرعينية]

<TABLE cellSpacing=0 cellPadding=8 width="100%"><TBODY><TR><TD>BACKGROUND
A 30-year-old man of Japanese descent presents to the emergency department (ED) after he had a syncopal event, which his wife witnessed. Apparently, he had several such episodes in the past, though he never sought medical evaluation for them. His wife states that they had been talking in the kitchen when her husband complained of feeling dizzy and nauseous. He then slumped over and fell out of his chair, hitting his head on the floor. Within a few seconds, he was awake and conversant. No tongue biting or jerky body movements were observed.

The patient is awake and alert, and his vital signs are stable. He does not have a specific complaint other than the bruise on his forehead and mild embarrassment. Electrocardiography is ordered (see Image). When you ask the patient if he has any family members who suddenly died at a young age, he mentions that his uncle died in his 30s without apparent cause.

What is the patient's underlying disorder and how is it treated? </TD></TR><TR><TD>Hint
ECG shows a specific precordial abnormality. Also consider the patient's family history of sudden cardiac death (SCD).</TD></TR></TBODY></TABLE>

[القصرعينية]

N.B.: this case needs search

[القصرعينية]

Brugada syndrome: The patient presents with syncope in the context of a family history of SCD. The vast majority of SCDs are due to ventricular fibrillation (VF) associated with structural heart disease, and SCD in the normal heart is uncommon, accounting for up to 5% of all cases. In patients with normal hearts, causes of SCD include Brugada syndrome, long-QT syndrome, preexcitation syndrome, and commotio cordis.

Brugada syndrome was originally described in 1992. It consists of the Brugada pattern on ECG and 1 or more of the following associated clinical features: syncopal episodes, documented VF, self-terminating polymorphic ventricular tachycardia (VT), family history of SCD in a relative younger than 45 years, and evidence of ST-segment elevation in family members.

The syndrome is characteristically caused by an autosomal dominant genetic defect resulting in the loss of function or dysfunction of the sodium channel. Brugada syndrome most commonly affects middle-age men (average presentation at 30 y) and can be recognized by its characteristic ECG pattern, ie, downsloping ST-segment elevation in leads V<SUB>1</SUB>-V<SUB>3</SUB> and QRS morphology resembling that of a right bundle branch block. Brugada syndrome can be distinguished from benign early repolarization (BER) in that the former has downsloping precordial ST-segment elevation, which is typically followed by a negative T wave, whereas the latter usually has a positive T wave. This patient has the characteristic ECG changes consistent with Brugada syndrome (see Image).

In the United States, the prevalence of Brugada syndrome is unknown. In some countries in Southeast Asia, the syndrome accounts for 40-50% of all cases of idiopathic VF.

A high index of suspicion should be maintained, especially when patients present with syncope in the setting of a family history of sudden death, even if their initial ECG is normal. Intermittent or concealed forms of Brugada syndrome can often be diagnosed by using the provocative administration of a class Ia antiarrhythmic, such as procainamide, in the electrophysiology laboratory. If the patient's history or ECG findings suggest Brugada syndrome, a cardiologist specializing in electrophysiology should be consulted. Not all patients presenting with syncope require admission. Patients who have had a syncopal episode in the setting of electrocardiographic abnormalities or family history of SCD (as in this case study) should be admitted to the hospital. An episode of VT/VF should prompt admission to a monitored setting, and early placement of a cardioverter-defibrillator should be considered. In addition, the treating cardiologist should arrange for an evaluation of the patient's family members, given the genetic pattern of autosomal dominance.

For more information on aortic dissection, see the eMedicine articles Syncope (http://www.emedicine.com/med/topic3385.htm) and Ventricular Fibrillation (http://www.emedicine.com/med/topic2363.htm) (within the Internal Medicine specialty).

The authors thank EMedHome.com (http://emedhome.com/) for permission to use their image.

References


Pinto DS, Josephson ME. Brugada syndrome and sudden cardiac death Available at: www.uptodate.com. Accessed February 8, 2005.
Antzelevitch C. The Brugada syndrome. J Cardiovasc Electrophysiol 1998;9:513-6.
Chen Q, Kirsch GE, Zhang D, et al. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature 1998;392:293-6.
Gussak I, Antzelevitch C, Bjerregaard P, et al. The Brugada syndrome: clinical, electrophysiologic and genetic aspects. J Am Coll Cardiol 1999;33:5-15.
Jones R, Gage A. Brugada syndrome as the cause of syncope in a 49-year-old man. Ann Emerg Med 2000;36:2.
Tintinalli JE. Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill; 2004.
Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128-35.