Empyema

 

Empyema

PKGhatak, MD

Empyema is defined as an accumulation of pus in the pleural space.

The surface of the lung and the inner surface of the chest wall is lined with a thin layer of serous tissue, leaving a minimal space in between known as pleural space. The pleural membrane is covered by just one layer of mesodermal epithelium upon a connective tissue layer consisting of collagen and elastic fibers. A thin film of pleural fluid bathes both the parietal (chest wall) and visceral(lung) pleura and acts as a lubricant; that makes the lungs expand and contract without any friction during breathing. The pleural fluid is formed by the parietal pleura and the fluid is removed by the lymphatics of this layer, so pleural fluid formation and removal go on continuously. The visceral pleura gets its blood supply from the bronchial arteries and has no sensory nerve supply, so the visceral pleura is pain insensitive, whereas, the parietal pleura is richly supplied with pain fibers from the intercostal nerves and also receives blood supply from the intercostal blood vessels.

In pneumonia usually, more fluid is formed in the pleural space, but the presence of fluid is not easily detected by examination or by simple chest x-rays. CT scan can detect in 15 to 30 % of cases minimal pleural effusion called Parapneumonic pleural effusion. As pneumonia resolves, so also the parapneumonic pleural effusion.

About 6 % of children and 5% of adults with community acquired pneumonia develop parapneumonic empyema. When pleura effusion is infected by the extension of infection, the fluid becomes cloudy and thick. If the infected fluid has the following characteristics, then the effusion is called Empyema: fluid pH is less than 7.2 (normal blood pH is 7.4), glucose less than 60 mg/dl. LDH is three times the upper limit of serum LDH or LDH over 1000 IU/dl, WBC over 50,000/ml, protein over 3,000 mg/dl. Gram stains identify the presence of bacteria.

Risk factors.

In children, empyema often results when pneumonia is treated with inappropriate antibiotics. For those who are not fully immunized, chickenpox is followed by pneumonia, and the use of Ibuprofen in pneumonia.

In adults, the risk factors are homelessness, pulmonary emphysema, Pulmonary tuberculosis, IV drug use, not receiving pneumonia vaccine, alcoholics, HIV infection, and immunosuppression by disease or therapy, and lung abscess. 35 % of anaerobic lung access is associated with empyema.

Both adults and children are at risk of empyema following prolonged chest tube drainage of bloody pleural effusion from a gunshot wound of the chest/ lung, knife wound, or automobile accident resulting in lung contusion, rib fracture, or pneumothorax.

Post-Surgical Empyema.

Following lobectomy and pneumonectomy due to malignancy or other diseases, if the lung fails to fill up the pleural cavity, then prone to empyema. This may be a special problem in the removal of bullous lesions in emphysema patients. Other causes of Empyema are Bronchopleural fistula, esophageal pleural fistula, perforated duodenal ulcer, amoebic liver abscess, perforated colon diverticulitis, and peritonitis the infection may spread to the pleural cavity and foreign bodies in pleural space like infected fragments of a projectile.

Common bacterial empyema.

The common bacteria is Streptococcus pneumonae type1. In community acquired pneumonia, the Streptococcus pneumonae type1 accounts for nearly 50% of postpneumonic empyema, Staphylococcus aureus followed by anaerobic bacteria infections. Viral parapneumonic and tubercular pleural effusion may also lead to empyema.

Symptoms and Diagnosis.

Persistent temperature elevation- often to 101F or higher, shortness of breath, chest pain, weight loss, anorexia, and general debility are common symptoms. On examination decreased or absent breath sound on one side of the chest, dullness on percussion. Leukocytosis with a shift to the left, toxin granules and Doehle bodies in the neutrophils are present. Chest x-ray shows pleural fluid. Ultrasound detects and delineates empyema easily and is usually repeated for monitoring purposes. CT chest is helpful in trauma cases and also in difficult cases.

Diagnostic thoracentesis is almost universal in all cases of more than minimal pleural effusion. In empyema, the pleural fluid is thick, difficult to aspirate, and cloudy to milky white. The other features will match the characteristics listed above.

Empyema fluid is sent to the lab for aerobic and anaerobic cultures and also for fungi and mycobacteria cultures. Gram stain of empyema fluid shows the presence of bacteria.

Treatment.

Closed tube drainage with a vacuum assisted closure device is inserted by Thoracoscopy. A wide bore chest tube Malicote 10-14F, Pigtail 8 -12F, or 28-32F French catheter is generally suited. Thoracoscopy can also detect septa, loculation, compartmentalization of fluid and that can be removed at the same time. That makes empyema drainage easier. Thoracoscopic lysis of adhesion is generally repeated.

Fibrinolytic enzymes like deoxyribonuclease DNase or tissue plasminogen activator tPA are injected into the pleural cavity and usually repeated in order to liquefy thick fluid.

Antibiotics are administered by IV and guided by culture and sensitivity tests.

In closed tube drainage of empyema, the lung should expand fully in 14 days.

If the lung fails to expand then re-culture of fluid, review of the entire case, use of multiple antibiotics, or other surgical measures are called for.

Open drainage.

If the empyema fluid is so thick that even the French 32 size catheters are not draining fluid then a wide area of the wound is created over the empyema. A large bore chest tube is inserted in the dependent part of the empyema and the other end of the tube is drained into a colostomy bag. The cavity is irrigated daily with mild antiseptic fluid, or the cavity is packed with saline moistened surgical gauge and changed daily. The cavity size should decrease gradually and the wound should seal in 4 to 5 months.

Open flap or Eloesser flap.

In this procedure, a wide incision is made just over the diaphragm, the most dependent part of the pleural cavity. A large skin and muscle flap is created. 1 to 3 ribs are resected to make a large opening into the chest cavity and the skin-muscle flap is stitched in a way creating a one-way opening for drainage making drainage of empyema easier. One way flap prevents air entry at the same time empyema is drained.

Decortication.

In the previous generation, tubercular empyema was the primary reason for this surgical operation. But occasionally some empyema fails to heal by the above methods and decortication is required.

If the lung does not expand to fill the chest cavity in 140 days. This procedure is considered. It is a major open thoracic surgery procedure, and many sick patients may not be able to withstand this procedure.

In this procedure, the entire pleura is stripped away and all cellular/fibrinous materials are removed. The lung with stripped away thick covering expands readily and the operative wound heals in 3 to 4 weeks.

The incidence of empyema has been declining over the past decades but in recent years the empyema incidence began creeping upwards. Early diagnosis and proper closed drainage and antibiotic therapy should resolve empyema in 2 to 3 weeks. The decision to open drainage of Empyema should be made after a thorough review of therapy and should be delayed until it is proven to be the only option available.

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Science of High Altitude Pulmonary Edema.

 

Science of High Altitude Pulmonary Edema

PKGhatak, MD

Airlines are carrying a large number of people to high altitude sky resorts and mountain climbing facilities. These popular recreational activities also put people at risk of mountain sickness and acute pulmonary edema.

At sea level, the partial pressure of oxygen (Pio2) in the air is 160 mm Hg. At 8,000 ft the Pio2 is 120 mmHg, at 11,000 ft. above sea level the Pio2 is 87 mmHg, and at extreme high altitude, 18000 ft., the Pio2 is only 50 mm Hg.

At any altitude above 4,000 ft. the blood level of oxygen is low and becomes lower at higher and higher altitudes.

Air enters the alveoli of the lungs with inhalation. On the way to the alveoli, the air becomes fully saturated with water vapor. At a body temperature of 98.8 degrees F, the partial pressure of H2O is 47 mmHg, PiO2 is diluted as air enters the alveoli and Pi02 becomes (160-47) 113 mmHg. The blood in the capillary is separated from the alveolar air by only one layer of cells. The oxygen(O2) of air first gets dissolved in the alveolar fluid and then rapidly binds with hemoglobin of blood because of the high affinity of oxygen to hemoglobin and forms loose compound oxyhemoglobin. The mixed venous blood Pvo2 is 40mmHg, favoring oxygen flow toward the blood due to a pressure gradient of 83 mmHg (113- 40).

When this is happening carbon dioxide (CO2) of blood is moving in the opposite direction – from blood into the alveoli, again due to the pressure gradient of 40 mmHg of blood to the + 0 mmHg of alveolar air. The CO2 binding is accelerated by the presence of enzymes- carbonic acid anhydrase. As little as 2 to 10 mmHg pressure gradient CO2 can move rapidly and completely.

As the blood leaves the alveoli and returns to the left side of the heart, the O2 carrying capacity of blood is at maximum – the PaO2(partial pressure of arterial blood) is over 90 mmHg and the O2 saturation (O2 sat) is 98 to 100 %.

Let's look at what happens at 8,000 ft. The Pio2 in the alveoli is 73 mmHg (120 – 47). The O2 gradient is (73-40) 43 mmHg. At 43 mmHg, the O2 sat is 75 %. This is significant Hypoxemia and patients immediately develop symptoms.

Effects of Hypoxia on Local Population.

The people living in the high plateau of Tibet for over 35000 years. The average altitude of the Tibetan plateau is 11,000 ft. They have developed an advanced adaptive mechanism, and it stands in contrast to the rest of high altitude residents of Ethiopia and Andes Mountain people. In Peru and Bolivia, the present population moved in about 1,100 to 800 years ago and has yet to adopt the full high altitude mechanisms of the Tibetan population.

In Peruvians and Bolivians, the hemoglobin level is higher due to the increased Erythropoietin activity, the minute ventilation is decreased, pulmonary arterial pressure is higher, right ventricular hypertrophy is present, Nitric Oxide(NO) levels are lower compared with Tibetan. They have more complications during pregnancy and childbirth, and newborns have lower weight at birth.

In Tibetan the mutation of EGLN1 and EPAS1 genes carry the adaptive oxygen sensing and high altitude hypoxic adaptive mechanisms. The hypoxic stimuli of carotid and aortic bodies are muted. There is no hyperventilation. At 85 mmHg, the O2 saturation of the air is over 87%, the nitrogen oxide levels in the lungs and blood are high. The hemoglobin levels are not elevated. The resting ventilation is high, and lung volumes are larger. The smooth muscles of the pulmonary artery are not hypertrophic, pulmonary hypertension does not happen. The weight of newborns is normal.

Effect of Hypoxia on Recent Arrivals.

Acute Mountain Sickness.

On the very day of arrival, symptoms of cerebral anoxia develop. The main symptoms are headaches, dizziness, nausea, anorexia, fatigue and shortness of breath on minimal activities, difficulty sleeping and mild dry cough. Swelling of face, hands and feet develop.

High Altitude Pulmonary Edema (HAPE).

From day 2 to day 4 of arrival, the symptoms are more severe. The shortness of breath at rest develops. The temperature rises to 101F degrees. Palpitation and rapid breathing, mental confusion, incoordination and prostration soon appear. The cough becomes productive of pink frothy sputum and occasionally becomes bloody, labored breathing with gurgling sounds on breathing is heard, cyanosis, and slow heart rate and BP began to fall. Acute respiratory distress and Acute Pulmonary edema set in.

High Altitude Cerebral Edema (HACE).

Anoxia of the brain cells is responsible for increased fluid accumulation in between brain cells and produces persistent headache, dizziness, nausea, the sensation of pins and needles, lethargy, incoordination, loss of sleep, tinnitus, violent behavior and loss of consciousness and seizures.

Pathophysiology of HAPE.

1. Hypoxia producing capillary leaks.

The tight junctions between the type I alveolar cells prevent excess fluid accumulation in the alveolar space. A thin layer of fluid is essential for the normal function of ventilation and gas exchanges. The integrity of the alveolar membrane depends on oxygen; in the hypoxic condition, the alveolar type I cells develop gaps between cell junctions and fluid escape in the alveolar space. Nitric oxide production is reduced, lack of nitric oxide in the lung results in smooth muscle contraction of pulmonary arteries and Pulmonary arterial BP (PBP) is elevated. That produces Right heart strain and hypertrophy. Dr. J.B. Web described the genesis of the capillary leak “The hydrostatic stress that exceeds the load bearing limits of the collagen network [of alveoli] results in rupture of the basement membrane.”

2. Derailed removal of fluid.

Two separate but interrelated paths are present in the lung to ensure fluid removal- these are

A. Starling force driven sodium channels.

B. Na and K iron ATPase dependent trans-epithelial sodium channels.

The functioning of both these channels is defective in hypoxic conditions.

If the foramen ovale was not completely closed the opening of the foramen ovale enlarges and the Right to Left shunt takes place which makes hypoxia more profound and early right heart failure develops. Endothelin1 activities are reduced and contribute to Pulmonary BP elevation.

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 C. Increase in pro-inflammatory markers in the lung.

Analysis of bronchial fluid obtained during the Intubation of HAPE patients show an increase in pro-inflammatory markers namely interleukin IL-1 beta, IL6, IL8, TNF alpha. In addition, the total cell counts are elevated, and increased lung macrophages are present. Blood levels of LDH, CRP, and total proteins are increased. The monocytes attractive protein1alpha (MIPA1alpha) and monocytes chemo-attractant protein1 and IL8 are significantly higher in Chronic Mountain sickness.

D. The anti-inflammatory markers- IL alpha, IL-10, show no change or levels are decreased.

Chronic Mountain Sickness.

Prolonged stay at high altitude results in the continuation of acute symptoms, in addition, the patients develop sleep disorders. Mental confusion, abnormal behavior, cognitive impairment and various neurological symptoms.

Returnee of Native of High Altitude.

High altitude people living on a lower plane for an extended period and then on returning to high altitude experience a more severe form of acute Pulmonary edema. The basic reason for this disease is not known.

Diagnosis of HAPE.

Respiratory symptoms in recent arrivals at high altitudes should always alert the possibility of acute mountain sickness or HAPE. This is the primary diagnosis and other possibilities like cardiac failure, PE, and pneumonia should come later.

Shortness of breath at minimal effort, or at rest, temperate elevation, frothy pink sputum, air hunger, cyanosis, tachycardia, and increased rate of respiration are universally present. Moist sounds, rales, on auscultation on both sides, chest x-rays- bilateral mid-zone, bat wing shaped infiltrates, and a low O2 saturation by pulse oximetry should be diagnostic of HAPE.

 

Immediate oxygen is administered by any available source to keep the O2 sat over 90%. Portable Hyperbaric oxygen chambers are generally available or should be made available as soon as possible. An arrangement must be made to take the patients to a lower altitude to a better medical facility.

Medications.

Nifedipine 20 mg tablets are given at 4 hourly to lower Pulmonary hypertension (PAP). Acetazolamide, a diuretic, also lowers PAP by blocking calcium channels, Tadalafil, a phosphodiesterase inhibitor, is also used. A bronchodilator Salmeterol is used to ease breathing.

Dexamethasone is used when cerebral edema is suspected in HAPE with predominate cerebral symptoms.

Prevention of acute mountain sickness and HEPA.

People should consult mountaineering school/ training centers at the time of preparation for such events. The day before arrival Nifedipine 80 mg long acting tablets one tablet and on arrival day and onwards one tablet should be taken. No physical activities on the 1^st day. Sleeping at a lower altitude should be considered. Daily hiking/climbing should be limited to 1500 feet.

Use portable oxygen when the pulse oximeter shows saturation below 90 %. And seek advice from the team leader or the guide.

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