Introduction:
Post operative acute negative pressure pulmonary edema is a consequence of alterations in the fluid dynamics in interstitial space of lung due to sudden changes in airway pressures and lung volumes.
The incidence of negative pressure pulmonary edema (NPPE) is reported to be 0.05% - 2% of all anesthetics. (most common in young patients with muscular built, greater force generation). The Australian incident monitoring study of 4000 incidences of laryngospasm during anesthesia showed that NPPE occur in up to 4% of all incident reports of laryngospasm. NPPE was first demonstrated in 1927 by Moore in spontaneously breathing dogs exposed to resistive load1.  The first description of the pathophysiological correlation between creation of negative pressure and the development of pulmonary edema was in 1942 by Warren et al2.
Type I NPPE develops immediately after onset of acute airway obstruction and Type II NPPE develops after the relief of chronic upper airway obstruction. The incidence of developing Type I NPPE associated with acute postoperative upper airway obstruction is 9.6–12%, whereas the incidence of developing Type II NPPE is 44%. In adults about 50% of NPPE occurrences are due to postoperative laryngospasm.

Causes of negative pressure pulmonary edema:

Pathophysiology:
Capillary blood is separated from alveolar gas by a series of anatomic layers: capillary endothelium, endothelial basement membrane, interstitial space, epithelial basement membrane, and alveolar epithelium (of the type I pneumocyte). The pericapillary perialveolar interstitial space is continuous with the interstitial tissue space that surrounds terminal bronchioles and vessels, and both spaces constitute the connective tissue space of the lung. There are no lymphatics in the interstitial space of the alveolar septum. Instead, lymphatic capillaries first appear in the interstitial space surrounding terminal bronchioles, small arteries, and veins. Between the individual endothelial and epithelial cells are holes or junctions that provide a potential pathway for fluid to move from the intravascular space to the interstitial space and finally from the interstitial space to the alveolar space. The fluid movement across the capillary endothelium is governed by Frank Starling equation, (net difference between colloid oncotic pressure of capillary and hydrostatic pressure of interstitium). Hence, there is propensity for fluid diffusion at lung zones 2 and 3, where as fluid resorption in zone 1. There is a negative pressure gradient between the perialveolar interstitium and peribronchial perivascular interstitium by virtue of its relation with peribronchial pleural invagination. Under normal circumstances, this causes movement of fluid, which has transuded across the perialveolar capillaries into lymphatics by sump mechanism. The sump mechanism is aided by the presence of valves in the lymph vessels, which allows unidirectional flow of fluids. The lymphatic fluid ultimately is drained into the venous system via thoracic duct. The increase in central venous pressure and the increased rate of fluid transudation into interstitium beyond the clearance capacity of the lymphatics lead to interstitial edema3.
In type I negative pressure pulmonary edema, forced inspiration against closed upper airway (peak inspiratory pressure of -50 to 100 cm of H2O) leads to increased transpulmonary gradient leading to increased fluid movement into the interstitium.
Mechanical damage of capillaries leads to intra alveolar movement of fluids.
Sympathetic stimulation due to resulting hypoxia, hypercarbia lead to pulmonary vasoconstriction further favouring formation of interstitial edema.
Increase in intrathoracic pressure leads to sudden and profuse increases in right ventricular preload leads to increase in pulmonary capillary pressure and displacement of interventricular septum towards left thus reducing he size of left ventricle. The reduction in  left ventricular volume along with increased intrathoracic pressure significantly increases the left ventricular end diastolic volume leading to decreased pulmonary outflow4.

In case of type II NPPE, In chronic upper airway obstruction there is a modest level of Auto positive end-expiratory pressure (PEEP) with an increase of end expiratory lung volume. When this chronic obstruction is relieved acutely, the Auto PEEP will disappear, the lung volumes and pressure return to normal, creating a negative intrapulmonary pressure, and if it is severe enough it will result in transudation of fluids in the lung interstitium and alveoli. This type of edema is called Type II NPPE. Presence of cardiac anomalies may predispose to occurrence of NPPE2.

Clinical features:
Usually, POPE develops immediately or within minutes after intubation or extubation of the trachea. Sometimes, however, symptoms and signs of POPE do not appear for several hours, prompting some physicians to advise up to 18 hours of close surveillance for patients who have had significant perioperative or out-of-hospital obstructive events.
A child or adult has hypoxemia, prolonged expiration, wheezing, and rales, with or without signs of bilateral pulmonary infiltrates.
Pink, frothy tracheal secretions accumulate suddenly after tracheal intubation for acute or chronic upper airway obstruction.
Oxygenation deteriorates after resolution of acute laryngospasm
or removal of a foreign body, the more rapid the onset of the obstruction,
the more severe the associated acute pulmonary edema.
The typical chest radiograph will show diffuse interstitial and alveolar infiltrates. NPPE has a characteristic appearance in Computed tomography (CT). Unlike other forms of pulmonary edema, computed tomography sections displayed a striking preferential central and nondependent distribution of ground-glass attenuation (edema/hemorrhage), which parallels the pleural and interstitial pressure gradients.
Predisposing factors: Anyone strong enough (male gender, in particular) to generate significant sustained negative intrapleural pressure against a closed glottis (Müller’s maneuver) or severely restricted upper airway is at risk for the development of NPPE. Factors predisposing to laryngospasm such as recent upper respiratory infection, dry cough and history of reactive airway disease, lighter planes of anesthesia, blood and secretions in throat may precipitate NPPE5.

Differential diagnosis:
Common differential diagnoses include aspiration pneumonitis and other causes of increased capillary permeability edema (e.g., fat or amniotic  fluid embolism, sepsis, cardiogenic causes, iatrogenic fluid overload). Acute pulmonary edema has also been reported in patients with head injury, heroin or other narcotic overdose, overly abrupt reversal of intraoperative narcotics (e.g.,using 400 μ g of naloxone as opposed to 20- to 40-μ g increments), venous air embolism, pulmonary embolectomy, and high-altitude exposure.

Management:
After recognition, management includes maintenance of a patent airway and the provision of adequate arterial oxygenation. Supplemental O2  is required, with or without continuous positive airway pressure (CPAP) or mechanical ventilation with PEEP. Tracheal intubation or reintubation is necessary to sustain the airway in 85% of adults and children. Slightly more than 50% of adults and just under 50% of children require mechanical ventilation4.
Additional measures include sedation, and muscle relaxation if required (when on mechanical ventilation). Diuretics and vasoactive drugs are indicated when there is severe pulmonary edema with co existing cardiac disorders.  Meanwhile other causes of pulmonary edema should be ruled out by assessment of the patient2,4.

Prevention:

1. Use of bite blocks to prevent patients from biting and obstructing the endotracheal tube while attempting to inhale at the same time.
2. Avoidance of factors that cause laryngospsam:
1. repeated failed attempts at endotracheal intubation (“Woody Woodpecker” syndrome)
2. inadequate anesthetic depth or skeletal muscle relaxation for tracheal intubation
3. excessive oropharyngeal secretions
3. Careful timing of tracheal extubation after general anesthesia to avoid stimulation during the excitement phase
4. The immediate, judicious use of CPAP after tracheal intubation or extubation in patients at high risk for POPE might mitigate the severity of the syndrome and minimize the need for reintubation and mechanical ventilation.

References:

1. Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: laryngospasm. Qual Saf Health Care 2005;14:e3.
2. Balu Bhaskar, John F. Fraser. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi Journal of Anaesthesia 2011; 5(3): 308 – 13.
3. William C Wilson, Jonathan Benumof. Physiology of the airway. In; Benumof and Hagberg’s Airway Management. 3rd edn. Eds: Carin A. Hagberg. Elsevier Saunders, Philadelphia. 2013: 143.  
4. Kenneth W Travis, John L Atlee. Post obstruction pulmonary edema. In; Complications in anaesthesia. 2nd ed. Ed: John L Atlee. Saunders, Philadelphia. 2007: 213 – 16.
5.  Ghofaily LAl, Simmons C, Chen L, Liu R. Negative Pressure Pulmonary Edema after Laryngospasm: A Revisit with a Case Report. J Anesth Clin Res 2012;3 :252.