Showing posts with label respiratory. Show all posts
Showing posts with label respiratory. Show all posts

Tuesday, October 16, 2012

PERCUTANEOUS TRACHEOSTOMY

Important summary of my presentation:
Since Ciaglia et al. described the percutaneous dilatational tracheostomy (PDT) in 1985, PDT has gained popularity over surgical  tracheostomy in the intensive care setting. Percutaneous tracheostomy (PCT) requires less time to perform, it is less expensive and it is typically performed sooner (because an operating room does not have to be scheduled).  In a meta-analysis of 17 randomized control trials, PDT offers several advantages such as decreased wound infections, decreased bleeding and mortality compared to surgical technique. Indications for PCT are the same as those for standard open tracheostomy. Established contraindications against PCT are unstable fractures of cervical spine, severe local infection of anterior neck and uncontrolled coagulopathy. Relative contraindications are high PEEP or oxygen requirements, difficult anatomy, proximity to extensive burns or surgical wounds, elevated intracranial pressure, haemodynamic instability and previous radiotherapy to the neck.  In experienced hands, PDT seems to be a safe procedure. The number of relative contraindications to PDT declines with increasing operator experience. Overweight patients have a five times higher risk of perioperative complications with PDT than normal weight patients.

Percutaneous tracheostomy using the dilator (or Ciaglia) technique is superior to other percutaneous approaches including the single-forceps (Griggs) technique. Several commercial kits are available for PDT. Eventhough procedure differs slightly with choice of kit, the basic steps remain common. No strong evidence supports one specific kit or technique. To minimize complications, it is recommended that each institution chooses one kit and gain familiarity to appreciate its advantages and drawbacks. With bronchoscope guidance, the operator can ascertain correct tracheostomy site, intratracheal guidewire placement, intratracheal dilator placement without tracheal damage, proper partial withdrawal of the endotracheal tube and placement of tracheostomy tube. If ultrasound machine is available, a skilled operator can evaluate the anatomy of major vessels and the thyroid gland in relation to tracheostomy site. It helps in localize the level of tracheal rings and indentify midline puncture, depth etc. Following PDT, a routine chest radiograph is probably unnecessary, provided the procedure had been uncomplicated. In a retrospective review of 60 patients undergoing tracheostomy with bronchoscopic guidance, a post-procedure chest radiograph was only useful in detecting complications following procedures deemed difficult by and experienced operator.

 

Saturday, October 13, 2012

Pulmonary Disease in Chronic Liver Failure

Portal hypertension is responsible for:
1. Gastrointestinal bleeding
2. Ascites
3. Portosystemic encephalopathy
4. Hepato-renal syndrome
5. Pulmonary disease:
    a. Hepato-pulmonary syndrome
    b. Porto-pulmonary hypertension

A. Hepatopulmonary syndrome
It is characterized by:
i. Portal hypertension (with or without cirrhosis)
ii. Hypoxaemia (A-a gradient > 15 mmHg on room air)
iii. Evidence of pulmonary vascular dilatation

Diagnosis: Contrast enhanced echocardiography demonstrates delayed  visualization of microbubbles (more than 3 cardiac cycles) into the left heart of injected agitated saline bubbles intravenously. This suggests intrapulmonary shunt, whereas immediate visualization would suggest intracardiac shunting.

Treatment: Oxygen therapy, exclusion of other causes of hypoxaemia (shunt) and liver transplant

B. Portopulmonary hypertension

It is characterized by:
i. Portal hypertension
ii. PCWP < 15 mmHg
iii. Pulmonary hypertension (mPAP > 25 mmHg at rest)
iv. Pulmonary vascular resistance > 120 dynes per m-5 (3 Woods units)

Diagnosis: Right heart catheterization with measurement of PAP is the 'gold standard for diagnosis.

Treatment is a liver transplant (LT). In appropriately selected subjects, LT can effectively treat all the complacations of endstage CLD. LT can be determined by calculation of the model for end-stage liver disease (MELD) score. It is contraindicated in severe pulmonary hypertension (mPAP > 50 mmHg) but can be considered in those who respond to treatment with oral or IV vasodilator therapy.

Reference: Manual of Intensive Care by Irwin and Rippe.

Questions: Forty year old man with history of hepatitis C presents with dyspnoea. On examination he is jaundiced, with spider naevi and ascites. Chest X-Ray and spirometry are normal. Pulse oximetry is performed: Standing 88% and Supine 97%. (From data interpretation in critical care medicine)

1. What is the likely diagnosis?
     Answer: Hepatopulmonary syndrome in end-stage Hep C cirrhosis.

2. What is the postulated pathophysiological mechanisms?
     Answer: Intrapulmonary vasodilation with right to left shunting. The process affects mainly the bases. Changes in posture that increase basal pulmonary blood flow (upright position) worsen gas exchange.

Orthodeoxia is hypoxaemia accentuated in the upright position.
Platypnoea is increased dyspnoea in upright position, improved by assuming the recumbent position. Causes are: a. Intracardiac shunts (intra-atrial shunt) with or without lung disease and b. Pulmonary vascular shunts (pulmonary artery-pulmonary vein communications) either anatomical or parenchymal.

3. What further investigation is indicated?
     Answer: see above

4. Is liver transplantation likely to help?
    Answer: Yes, over 80% of patients with hepatopulmonary syndrome have resolution or marked improvement in intrapulmonary vasodilatation with LT. This contrasts with portopulmonary hypertension which is considered a contraindication (see comment above).




 

Monday, April 4, 2011

High frequency ventilation

Currently HFOV is used as salvage therapy for patients failing conventional mechanical ventilation. It should restricted to centres with training and experience in this mode of ventilation. HFOV provides tidal volume below the anatomic dead space at frequencies greater than 60 breaths per second.

Benefits include reduce barotrauma, improve V/Q matching and less respiratory compromise. Complications include dessication and inspissation of mucus, airway damage due to high gas velocities, air trapping and high shear forces at interfaces between areas of the lung at different impedences.



Gas exxchange during HFOV:



  • direct bulk flow


  • longitudinal (taylor) dispersion


  • pendeluft


  • asymmetric velocity profile


  • cardiogenic mixing


  • molecular diffusion


1. Two observational studies, adults who failed to respond to conventional ventilation were managed with HFOV at 5 Hz. Improvement in oxygenation were noted within 8 hours in both studies. (Fort CCM 1997, Mehta CCM 2001).


2. HFOV for ARDS in adults: a RCT. Derdak AJRCCM 2002.

Multicentre Oscillatory Ventilation for ARDS Trial (MOAT)

148 adults were randomised to HFOV or conventional ventilation. The HFOV group had significant improvement in oxygenation within 16 hours,compared to conventional ventilation. However the improvement did not persist and oxygenation was the same in both groups by 24 hours. The survival trend favour HFOV over CV but is underpowered (would need n=199 to evaluate mortality)


The difference in survival rate did not reach significance at 30 or 90 days.



3. High frequency oscillatory ventilation in adults: the Toronto experience. Mehta Chest 2004 Canadian experience, Retrospective chart review of 156 patients treated with HFOV. The authors suggested that HFOV might be an effective rescue therapy for patients with severe oxygenation failure. Because mortality was associated with a greater number of days receiving conventional ventilation prior to HFOV, the authors also suggested that earlier institution of HFOV could be beneficial.



4. High Frequency Oscillatory Ventilation Compared to Conventional Ventilation in ARDS: a RCT. Bollen et al. Crit Care 2005

ICU in London, Cardiff, Paris, Mainz. n = 61

Study stopped prematurely because of la ow inclusion rate and the completion of similar MOAT trial.

No difference in 30 day mortality. Post hoc analysis- better treatment effect of HFOV in patients with higer baseline oxygen index (OI).


Critics: Small number of patients, lack of explicit ventilation protocol and underpowered to show differences in efficacy or safety.


Conclusions:


1. HFOV as safe and efficacious as lung protective controlled ventilation in RCTs.

2. There is a trend of improved mortality with HFOV but this needs to be repeated in a fully powered, properly controlled RCT.

3. HVOV may be more effective in patients with high baseline OI, but this should be studied directly.




Sunday, March 27, 2011

Extracorporeal membrane oxygenation (ECMO)

1. Extracorporeal membrane oxygenation for 2009 Influenza (H1N1) ARDS - ANZ ECMO influenza investigators. Journal: JAMA, Oct 19, 2009 A descriptive analysis of all adult and paediatric (neonates excluded) patients treated with ECMO, 1st june - 31 August 2009 in Australia, NZ ICU's during 2009 H1N1 epidemic. In 200 ICUs, 15 supplied ECMO for 61 (32%) of 194 H1N1/ Influenza A ventilated patients with 21% mortality. All these patients met inclusion criteria for the CESAR trial. to be continued..

Saturday, February 12, 2011

Community Acquired Pneumonia

This week is another busy week since the third block of undergraduate medical students are starting their new session this coming Monday. I have to ensure the course guideline, log books and rosters are ready by then. I am just helping the department, yes the department (not MY department). I am having problem with someone, let me correct it not just me..at least there are two more members feel the same way......"Please" costs nothing, "Sorry" costs your pride, "I forgive you" liberates you from the shackles of prejudice.

The mortality of CAP patients admitted to ICU is about 35%. About 20% of patients admitted to ICU with CAP are in septic shock, with mortality as high as 60%.
The presence of comorbidities below contribute significantly to mortality and also alter the etiologic organisms underlying the infection.

  1. COPD
  2. asthma
  3. diabetes mellitus
  4. renal insufficiency
  5. congestive heart failure
  6. coronary artery disease
  7. malignancy
  8. alcoholism
  9. age>70years
  10. chronic nerological disease
  11. chronic liver disease
The most common pathogens are:
  1. Strep pneumonia
  2. Legionella species
  3. Staphylococcus aureus
  4. Haemophillus Influenza
  5. Gram negative bacilli
Pathogens associated with underlying comorbid condition:
1. S.pneumonia
  • Dementia
  • congestive heart failure
  • COPD
  • Cerebrovascular disease
  • Institutional crowding
  • seizures
2. Penicillin resistant and drug resistant pneumococcus
  • age>65
  • alcoholism
  • immunomodulating illness or therapy (including steroids)
  • Previous B lactam therapy within 3 months
  • Multiple medical comorbidities
  • exposure to child in day care centre
3. Enteric gram negatives
  • residence in long term facility
  • underlying cardiopulmonary disease
  • recent antibiotic therapy
  • multiple medical comorbidities
4. Pseudomonas aeruginosa
  • broad spectrum antibiotics for > 7 days in the past month
  • structural lung disease (bronchiectasis)
  • corticosteroid therapy
  • malnutrition
  • undiagnosed HIV infection
  • netropenia
5. Legionnaires' disease
  • AIDS
  • haematologic malignancy
  • end stage renal disease
Non infectious diseaseas masquerading as CAP should be excluded:
  1. Cryptogenic organizing pneumonia (COP)
  2. Eosinophilic pneumonia
  3. Hypersensitivity pneumonia
  4. Drug induced pneumonitis: methotrexate, nitrofurantoin, gold, amiodarone etc
  5. Pulmonary vasculitis
  6. PE/ infarction
  7. Pulmonary malignancy
  8. Radiation pneumonitis
  9. TB
The following are the major reasons for a failure to respond to anti microbial agents:
  1. Wrong antibiotic: wrong spectrum or drug resistance. Wrong dosage
  2. Viral, fungal, or opportunistic pathogen.
  3. Unusual pathogens
  4. Superadded complication
  5. Complicated pleural effusion/ empyema
  6. endocarditis
  7. Purulent pericarditis
  8. Septic arthritis
  9. Meningitis
  10. Exclude masquerader
  11. Consider CA-MRSA in toxic patients and those with severe disease.
Unusual pathogens
  1. Coxiella burnetii - cats, goats, sheep, cattle
  2. Tularemia - rabbits, ticks
  3. Leptospirosis -rats
  4. Hantavirus - rats
  5. SARS
  6. Psittacosis - birds
  7. Nocardia - steroids
  8. Aspergillus -steroids
  9. Pneumocystis jiroveci -immunosuppression
  10. Dimorphic fungi -recent travel
  11. Burkhodelria pseudomallei -recent travel
  12. TB
Complicated Pleural effusions -
drainage is necessary if the pleural fluid is grossly purulent or if pleural fluid show the following
  • pH less than 7.2
  • Glucose less than 2.2mmol/l
  • WCC > 10,000/ml

Monday, January 31, 2011

Comorbidities associated with delayed resolution of pneumonia

1. COPD
Impaired cough and mucociliary clearance
2. Alcoholism
Aspiration, malnutrition, impaired neutrophil function
3. Neurologic disease
Aspiration, impaired clearance of secretions and cough
4. Heart Failure
Edema fluid, impaired lymphatic drainage
5. Chronic Kidney disease
hypocomlementaemia, impaired macrophage and neutrophil function, reduced humoral immunity
6. Malignancy
Impaired immune function, altered colonization, effects of chemotherapy
7. HIV
Impaired cell mediated and humoral immunity
8. Diabetes Mellitus
Impaired neutrophil function and cell mediated immunity