Saturday, January 24, 2015

Atrial septal defect device closure

This procedure is called as Atrial septal defect (ASD) device closure.

Transesophageal echocardiography (TEE) is must before procedure for:
1) actual sizing of the defect
2) defining the rims - to hold device in place
3) ruling out anomalous pulmonary venous drainage
4) ruling out significant mitral regurgitation (MR).
Intraprocedural TEE is not mandatory.

N.B How to distinguish between an ASD device and a patent foramen ovale (PFO) device? Left atrial (LA) disk (green arrow) is larger than Right atrial (RA) disk (yellow arrow), thus it is an ASD device.For a PFO device, RA disk will be larger than LA disk.

Further readings:

Friday, January 23, 2015

A case of Mycobacterium marinum infection in a fisherman

Historically recognized as “swimming pool” or “fish tank” granuloma.

Clinical features:
Most infections occur 2 to 3 weeks after contact with contaminated water from one of these sources. The lesions are most often small violet papules on the hands and arms that may progress to shallow, crusty ulcerations and scar formation. Lesions are usually singular. However, multiple ascending lesions resembling sporotrichosis can occasionally occur.
Most patients are clinically healthy with a previous local hand injury that becomes infected while cleaning a fish tank or patients may sustain scratches or puncture wounds from saltwater fish, shrimp, fins and other marine life contaminated with
M. marinum. Swimming pools seem to be a risk only when non-chlorinated.

Diagnosis is made from culture and histologic examination of biopsy material, along with a compatible history of exposure.


No treatment of choice is recognized for M. marinum. However, successful treatments have traditionally been a two-drug combination of Rifampin (600 mg/day) plus Ethambutol (15mg/Kg) or monotherapy with Doxycycline, Minocycline (100 mg BD), Clarithromycin (500mg BD) or Trimethoprim-Sulfamethoxazole given for a minimum of 3 months. Clarithromycin has been used increasingly because of good clinical efficacy and minimal side effects, although published experience is limited.

The following is the case of a fisherman who got injured while handling his fishing cage and presented with extensive papular lesions on his forearm. He was started on two drug-combination therapy for 5 months.

The second image is the same patient after 3 months of treatment.

Monday, January 19, 2015


COPD exacerbation - definition, assessment, management

COPD exacerbation:

Exacerbation of COPD is defined as an acute episode, characterized by the worsening of the patient’s respiratory symptoms that is beyond normal daily variations and that will eventually lead to a change in his medications.
Those having 2 or more exacerbations per year are known as “frequent exacerbators”.

Precipitating factors:
1) Respiratory tract infections – viral or bacterial. Most common cause. There may be an increased bacterial burden in the lower airways or new strains of bacteria are acquired during an exacerbation. Commonly implicated viruses
include rhinovirus, respiratory syncytial virus, coronavirus and influenza virus.
2) Air pollution.
3) Interruption of maintenance therapy.
4) Unknown causes – 30% cases.

Diagnosis should be made clinically whereby the patient complains of an acute aggravation of his symptoms out of proportion to his day to day variations. 

Medical history:
1) Severity of COPD before this exacerbation
2) Duration of the worsening or any new symptoms
3) Number of previous exacerbations or hospitalizations
4) Associated comorbidities
5) Present medications
6) Previous uses of mechanical ventilation.
Clinical examination:
1) Use of accessory respiratory muscles or paradoxical chest wall movements
2) Development of central cyanosis or exacerbation of pre-existing cyanosis
3) Change in mental status
4) Development of peripheral edema
5) Hemodynamic instability

Tests to assess severity include:
1) Pulse oximetry – good for monitoring.
2) Arterial blood gases and acid base status – shows whether there is an acute or acute on chronic respiratory failure.
3) Chest radiography – excludes alternative diagnoses and can show infections.
4) EKG – may help to assess any pre-existing cardiac problems.
5) Complete blood count – white cells may be elevated, hematocrit may be elevated
6) Blood biochemistry.
Spirometry is difficult to perform during an exacerbation and it may not be of enough accuracy. Therefore it is not recommended.

More than 80% of cases can be managed as outpatients but if the following conditions are seen, it is better to admit and if necessary give intensive care:
1) Dyspnea occurring at rest
2) Old age
3) Frequent exacerbator
4) Failure of response to change in/addition of medication to control the exacerbation
5) New onset of arrhythmias or peripheral edema.

Medical therapy consists of:
1) Short acting inhaled bronchodilators – beta-2 agonists with or without anti-cholinergics are preferred. It is better to use a nebulizer as the patient usually is dyspneic and lacks coordination to inhale from a metered-dose inhaler. IV methylxanthines are considered as second line of therapy for bronchodilation and are to be used only in selected cases, especially if there is poor response to short acting inhaled bronchodilators.
2) Corticosteroids – oral prednisone 40 mg/day for 5 days has been shown to shorten recovery time and improve lung function as well as arterial hypoxemia.
3) Antibiotics – these are indicated if the patient has clinical signs of bacterial infections e.g. increased in sputum purulence.  Procalcitonin III may help to indicate antibiotic therapy as it is increased in cases of bacterial infections. Usually in the following conditions antibiotics should be considered:
- 3 cardinal symptoms present: increase in dyspnea, sputum volume and sputum purulence,
- 2 cardinal symptoms, with purulence being one of the symptoms,
Antibiotics are recommended for 5-10 days.
4) Adjunct therapies – proper control of comorbidities is advised. Thromboprophylactic measures should be enhanced.

Respiratory support:
1) Oxygen therapy: Oxygen is titrated to correct the hypoxemia of the patient aiming to achieve a saturation of 88-92%. Usually Venturi masks are preferred to nasal prongs. After 30-60 minutes of oxygen therapy, arterial blood gases should be checked.
2) Non-invasive mechanical support
3) Invasive mechanical support.

Friday, January 9, 2015

Hyperemesis gravidarum - definition, epidemiology, pathophysiology, complications, management

Mild to moderate nausea and vomiting are seen commonly until approximately 16 weeks in most pregnant ladies. Although nausea and vomiting tend to be worse in the morning, thus erroneously termed morning sickness, they frequently continue throughout the day. In some cases, however, it is severe and unresponsive to simple dietary modification and antiemetics.
Hyperemesis gravidarum is defined as vomiting sufficiently severe to produce weight loss, dehydration, alkalosis from loss of hydrochloric acid and hypokalemia. Rarely, acidosis from partial starvation and transient hepatic dysfunction develop.
Modified PUQE scoring index (Pregnancy-Unique Quantification of Emesis and Nausea) can be used to quantify the severity of nausea and vomiting. 

There appears to be an ethnic or familial predilection. The hospitalization rate for hyperemesis is around 0.5 to 0.8%. Hospitalization is less common in obese women. In women hospitalized in a previous pregnancy for hyperemesis, up to 20 percent require hospitalization in a subsequent pregnancy.

Hyperemesis appears to be related to high or rapidly rising serum levels of pregnancy-related hormones. The presumed culprits include human chorionic gonadotropin (hCG), estrogens, progesterone, leptin, placental growth hormone, prolactin, thyroxine and adreno-cortical hormones. Some studies have implicated the vestibular system while others have showed some involvement of psychological components.
Other factors that increase the risk for admission include
1) hyperthyroidism, 
2) previous molar pregnancy, 
3) diabetes, 
4) gastrointestinal illnesses and 
5) asthma. 
For unknown reasons, a female fetus increases the risk by 1.5-fold.

Vomiting may be prolonged, frequent and severe.
1) Various degrees of acute renal failure from dehydration are encountered.
2) Life-threatening complications of continuous retching include Mallory-Weiss tears shown in the figure below. Others are esophageal rupture, pneumothorax and pneumomediastinum.
3) At least two serious vitamin deficiencies have been reported with hyperemesis in pregnancy. Wernicke encephalopathy from thiamine (vitamin B1) deficiency is not uncommon. Vitamin K deficiency has been reported causing maternal coagulopathy and fetal intracranial hemorrhage.

The photo shows a Mallory Weiss tear with the endoscope in retroflexion.

1) Eating small meals at more frequent intervals but stopping short of satiation is valuable. The herbal remedy, ginger, was effective as showed by this meta-analysis published in 2014. Ginger capsules 250 mg 4 times daily.
2) A number of antiemetics given orally or by rectal suppository as first-line agents. When simple measures fail, intravenous crystalloid solutions are given to correct dehydration, ketonemia, electrolyte deficits, and acid-base imbalances. Thiamine, 100 mg, is given to prevent Wernicke encephalopathy. Diclegis (Doxylamine and Pyridoxine (Vitamin B6) ) is the only FDA approved medication for nausea and vomiting in pregnancy. 
3) If vomiting persists after rehydration and failed outpatient management, hospitalization is recommended. Antiemetics such as 
- Promethazine 12.5-25 mg 4 hourly, 
- Prochlorperazine 5-10 mg 6 hourly, 
- Metoclopramide 5-10 mg 8 hourly are given parenterally.
With persistent vomiting after hospitalization, appropriate steps should be taken to exclude possible underlying diseases as a cause of hyperemesis (gastroenteritis, cholecystitis, pancreatitis, hepatitis, peptic ulcer and pyelonephritis).

Further readings: