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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 3  |  Issue : 3  |  Page : 223-225

An anesthetic management of negative pressure pulmonary edema


1 Department of Anesthesia, IGIMS, Patna, Bihar
2 Department of Cardiology, JLN Medical College, Ajmer, Rajasthan

Date of Web Publication9-Jun-2016

Correspondence Address:
Dipti Raj
c/o Dr. Akhilesh Kumar Singh, House No: 59-b, Road No: 8-b, Rajendra Nagar, Patna - 800 016, Bihar

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2348-3334.183750

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  Abstract 

Negative pressure pulmonary edema (NPPE) is one of the common complications of upper airway obstruction seen by anesthesiologist during either in induction or emergence sometimes both. Patients who have experienced NPPE are generally healthy without comorbidities. NPPE is a result of marked decrease in intrathoracic pressure caused by ventilator efforts against a closed glottis resulting in disruption of normal intravascular Starling mechanism, leading to transudation of intravascular protein, and fluids into the pulmonary interstitium. The onset of NPPE is usually rapid and without prompt recognition and intervention, the outcome can be fatal. This case report is of a 40-year-old female adult, who underwent right-sided percutaneous nephrolithotomy for stone in the right kidney otherwise uncomplicated surgical procedure.

Keywords: General anesthesia, negative pressure pulmonary edema, percutaneous nephrolithotomy


How to cite this article:
Raj D, Priti K, Quari H, Jha RK. An anesthetic management of negative pressure pulmonary edema. CHRISMED J Health Res 2016;3:223-5

How to cite this URL:
Raj D, Priti K, Quari H, Jha RK. An anesthetic management of negative pressure pulmonary edema. CHRISMED J Health Res [serial online] 2016 [cited 2021 Sep 21];3:223-5. Available from: https://www.cjhr.org/text.asp?2016/3/3/223/183750


  Introduction Top


Negative pressure pulmonary edema (NPPE) can be a cause of life-threatening complication if underdiagnosed or left untreated. It can be either due to acute or chronic airway obstruction which can be misdiagnosed. The incidence of NPPE, as complications of all anesthetics, is said to be 0.05-0.1%. The mortality of an undiagnosed NPPE is as high as 40%. [1]


  Case report Top


A 40-year-old female patient, weight 60 kg, American Society of Anesthesiologists I Class 1 was scheduled for right-sided percutaneous nephrolithotomy. She did not have any associated comorbidity or any significant history in the past. Her routine blood investigations, chest X-ray, and electrocardiography (ECG) were within normal limits.

She was planned for general anesthesia. Patient was preoxygenated with 100% oxygenation for 3 min. General anesthesia was induced with fentanyl 2 mcg/kg, propofol 2.5 mg/kg, and vecuronium 0.1 mg/kg intravenously. The patient's trachea was intubated with cuffed endotracheal tube of size 8.5 mm. Anesthesia was maintained with O 2 , N 2 O (30:70), isoflurane, and vecuronium bromide. Intraoperatively, patient also received ondansetron 0.1 mg/kg intravenous (iv) and paracetamol 20 mg/kg iv. Perioperative monitoring included ECG, noninvasive blood pressure (NIBP), pulse oximetry, and end-tidal capnography.

The duration of surgery was 2 h and patient received 2 liters of Ringer's lactate. His urine output was approximately 500 ml. Neuromuscular blockade was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 0.01 mg/kg iv. The patient received diclofenac 75 mg intravenously for postoperative pain relief.

Postextubation patient developed stridor and became dyspneic and restless. Her pulse oximeter showed 80-85% of oxygen saturation. We adequately mask-ventilated the patient with anatomical face mask. Saturation improved to 85-90%. On chest auscultation, fine crepitations with occasional rhonchi were heard bilaterally. Patient developed tachycardia up to 120-130/min and NIBP was 130/80 mmHg. As suspecting a case of postoperative pulmonary edema, morphine 6 mg and furosemide 20 mg were given intravenously. Meanwhile, arterial blood gas (ABG) sampling was done, report suggested hypoxia, hypercarbia, and acidosis. A portable chest X ray was done for the patient confirming it to be a case of postoperative pulmonary edema [Figure 1]. Head end was elevated and iv fluids were restricted. Patient was shifted to Intensive Care Unit where he was put on continuous positive airway pressure (CPAP) by face mask with pressure support of 12 cm and PEEP of 6 cm of water was applied. Meanwhile, portable chest X-ray was done for the patient confirming it to be a case of postoperative pulmonary edema. Six hourly ABG was repeated. Patient saturation now improved to 96-97%. CPAP support was given to the patient for 24 h. Repeat chest x- ray showed resolving post operative pulmonary edema at 12 hour [Figure 2]. After that, repeat chest X-ray was done and showed clear lung fields and ABG reports were within normal limits [Figure 3]. On auscultation of the chest, bilateral air entry was equal and no added sounds were heard. After that, the patient was shifted to private ward same evening and discharged on the 7 th postoperative day.
Figure 1: Radiograph shows acute pulmonary edema after 1 h postoperative period

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Figure 2: Radiograph shows resolving pulmonary edema after 12 h postoperative period

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Figure 3: Radiograph shows normal findings after 24 h postoperative period

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  Discussion Top


NPPE is a noncardiogenic type. It is of 2 types. Type 1 is of sudden onset following upper airway obstruction, and type 2 develops after surgical relief of chronic upper airway obstruction. [2],[3] Both types of NPPE can present with acute respiratory distress. Type 1 usually occurs within 60 min of a precipitating event, [4] or it can take up to 6 h in some cases. [5] This condition requires rapid intervention and may be confused with other causes of postoperative respiratory distress. The presenting signs can be agitation, tachypnea, tachycardia, frothy pink pulmonary secretions, rales, and progressive oxygen desaturation. Chest X-ray findings of pulmonary edema support the diagnosis. The absence of gastric contents in pulmonary secretions, a history of normal cardiac functions, and particularly, the occurrence of such symptoms in a vigorous young person makes the diagnosis of NPPE more likely.

Extreme negative intrapleural pressure (peaks of sustained inspiratory pressure between 50 cm of H 2 O and 100 cm of H 2 0 though the mean basal pressure is around 4 cm of H 2 O) may trigger pulmonary edema. [3] Primary mechanism behind postobstructive pulmonary edema is hydrostatic forces. Here, the alveolar epithelium remains functionally intact in acute postobstructive pulmonary edema. [3]

Other reported causes are impacted foreign body in the trachea/bronchus, epiglottitis, strangulation, vocal cord palsy, inspissated tracheal secretions, goitre, suctioning of endotracheal tube, difficult intubation, upper airway tumor, hematoma, Ludwig angina, oropharyngeal surgery, hematoma, obesity, mediastinal tumor, biting/obstruction of endotracheal tube/laryngeal mask, falling back of tongue, croup, etc. [1]

The most common clinical presentation of NPPE is the occurrence of airway obstruction on emergence from general anesthesia followed by rapid onset of respiratory distress, hemoptysis, and clinical/radiological features consistent with bilateral pulmonary edema. Typically, NPPE radiologically manifests as Kerley lines, peribronchial cuffing, and in severe cases, as central alveolar edema. Cardiac size is usually normal as hypervolemia is not present. Resolution of clinical and radiological features is rapid, usually within 24 h. NPPE can be unilateral if the obstruction was previously at the level of right or left main stem bronchus. [6] It is generally seen after removal of endotracheal tube removal but NPPE also been reported after use of laryngeal mask airways. [7]

Differential diagnosis of NPPE includes aspiration pneumonitis, acute induced noncardiogenic pulmonary edema, and anaphylaxis.

The treatment is primarily supportive and includes maintenance of a patent airway and administration of supplemental oxygen.

Management of NPPE ranges from oxygen supplementation through a simple mask to mask CPAP, endotracheal intubation, and positive pressure ventilation with PEEP. Diuretics are often administered, but its role is uncertain in the management of NPPE. [8]


  Conclusion Top


NPPE due to obstruction in upper airways can aggravate low morbidity surgeries affecting mainly young patients. The knowledge of this complication, and most importantly, its prevention are crucial.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Saraswat V, Madhu PV, Kumar SS. Rapid onset acute epiglottitis leading to negative pressure pulmonary edema. Indian J Anaesth 2007;51:429.  Back to cited text no. 1
  Medknow Journal  
2.
Wadhwa R, Kalra S. Negative pressure pulmonary oedema after rhinoplasty. Indian J Anaesth 2010;54:363-4.  Back to cited text no. 2
[PUBMED]  Medknow Journal  
3.
Kapoor MC. Negative pressure pulmonary edema. Indian J Anaesth 2011;55:10-1.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.
Rasheed A, Palaria U, Rani D, Sharma S. A case of negative pressure pulmonary edema in an asthmatic patient after laparoscopic cholecystectomy. Anesth Essays Res 2014;8:86-8.  Back to cited text no. 4
  Medknow Journal  
5.
Koch SM, Abramson DC, Ford M, Peterson D, Katz J. Bronchoscopic findings in post-obstructive pulmonary oedema. Can J Anaesth 1996;43:73-6.  Back to cited text no. 5
    
6.
Kallet RH, Daniel BM, Gropper M, Matthay MA. Acute pulmonary edema following upper airway obstruction: Case reports and brief review. Respir Care 1998;43:476-80.  Back to cited text no. 6
    
7.
Sato F, Sato N, Hata Y, Suzuki A, Goto H, Otsuka H, et al. Negative pressure pulmonary edema during tracheal Dumon stent implantation. J Bronchology Interv Pulmonol 2012;19:345-8.  Back to cited text no. 7
    
8.
Vandse R, Kothari DS, Tripathi RS, Lopez L, Stawicki SP, Papadimos TJ. Negative pressure pulmonary edema with laryngeal mask airway use: Recognition, pathophysiology and treatment modalities. Int J Crit Illn Inj Sci 2012;2:98-103.  Back to cited text no. 8
[PUBMED]  Medknow Journal  


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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