Jadwiga Biernacka, Andrzej Nestorowicz, Krzysztof Kupisz, Ziemowit Rzecki
Pneumoperitoneum complicating resuscitation in the early postoperative period. Case report
Chair and Department of Anaesthesiology and Intensive Therapy,
Head: prof. A. Nestorowicz M.D., Ph.D.; Medical Academy, Lublin, Poland
We present a case of pnemoperitoneum that has developed itself after resuscitation during a recovery phase after a submandibular gland tumour resection. Pneumoperitoneum was caused by the gastric rupture, probably during resuscitation. Immediate diagnosis was made and subsequent surgery performed; patient recovered completely.
Postoperative complications are the adverse factors, which influence the overall results of otherwise uneventful surgery and anaesthesia. Complications of a general character (as opposed to local ones) may threaten the patient's life and require immediate therapeutic intervention. The overall rate of complications ranges from 3 to 4% of all anaesthesias. Not infrequently they are observed in patients with a relatively low operative risk .
Without any doubt, the most dramatic complication of the early postoperative period is cardiac arrest (CA). If it occurs, the supervising personnel (regardless of medical qualifications) is obliged to begin resuscitation procedures immediately, in order to restore the basic vital functions, as early as possible. Rapidly started artificial ventilation and external cardiac compression gives a chance of successful reanimation but can also be the cause of complications. The most common are: sternum and costal fractures; pneumo- and haemothorax; rupture of the liver, spleen or diaphragm and trauma to the heart.
The aim of this paper is to present a case of a very rare complication of resuscitation: pneumoperitoneum caused by a full-thickness gastric wall rupture.
A 75-year old male was qualified for excision of a tumour of the right submaxillary salivary gland under general anaesthesia. Preoperative examination did not reveal significant risk factors from the cardiovascular or respiratory system. The history showed well-controlled, stable arterial hypertension. Chest X-ray demonstrated primary tuberculosis sign (calcified) in the left lung and moderate pulmonary emphysema. ECG tracing was normal (regular sinus rhythm of 80/min.). Laboratory tests (blood cells count, electrolytes, liver tests, and coagulation) were in the normal range. Blood pressure equalled 140/80 mmHg (18.6/10.6 pa. The patient was classified as ASA grade II.
The patient was premedicated with hydroxizine 50mg i.m. At induction of anaesthesia he received thiopentone 5 mg/kg and suxamethonium 1 mg/kg. The maintenance of anaesthesia was carried out with N2O/O2 in 2:1 proportion, fractionated doses of fentanyl and alcuronium. The course of surgery (lasting 3.5 hours) and anaesthesia were uneventful. During the procedure, the patient received 0.6 mg of fentanyl and 40mg of alcuronium; 2000 ml of crystalloid solution was infused (estimated blood loss 250 ml). The last dose of opioid and a muscle relaxant was administered 60 minutes before the end of anaesthesia. After the operation, neuromuscular block was reversed with atropine 1 mg and neostigmine 2.5 mg. At this time blood pressure value was 150/80 mmHg (20/10.6 kPa), heart rate 72/min., regular sinus rhythm; the patient was fully conscious, breathing spontaneously and did not report any pain.
After about 20 minutes after transferring the patient to the Department of Laryngology, cardiac arrest occurred. The external cardiac massage and artificial ventilation were started immediately, first as a mouth-to-mouth breathing then with a face mask and an AMBU bag. The anaesthesiologist team, called to the ward, intubated the patient. All vital functions were maintained by basic life support procedures. During resuscitation the patient received adrenaline 2 mg i.v. in fractionated doses. After 15 minutes spontaneous heart function returned (sinus rhythm 120/min.) demonstrating single supra- and ventricular extrasystole. Blood pressure measured was 140/90 mmHg (18,6/12 kPa). Peripheral oxygen haemoglobin saturation, assessed by pulsoxymetry, was 99%, during AMBU bag ventilation with continuous oxygen flow at the rate of 6 l/min.
Because of marked abdominal distension an attempt to insert a nasogastric tube was made. This proved unsuccessful, even with an aid of an oesophagoscope, as the tube could not be passed by the cardia. Endoscopy was performed again in the operating theatre under general anaesthesia: it did not reveal gas or pathologic changes in the stomach.
General condition of the patient was systematically worsening, with increasing abdominal distension. No pulse over the left femoral artery was present, without the symptoms of acute limb ischaemia. On physical examination, rales over both lungs were present, as well as elevation lung borders. Heart rate increased and blood pressure decreased. Chest and upper abdominal X-ray revealed the presence of the air under both diaphragm domes. On the basis of these findings the patient was qualified for an emergency laparotomy.
Under general anaesthesia (O2, fentanyl, pancuronium) the abdominal cavity was opened. At the opening the pneumoperitoneum evacuated spontaneously.
No diagnosis was done during inspection or palpation of abdominal organs. A 3-cm long tear of the posterior stomach wall was found only after filling the peritoneum with saline solution and instilling air via the nasogatric tube. It was localised in the mid-body portion, proximally to the minor curvature (Fig.1). The tear was closed in two layers. A drain was left at the proximity of the epiploic foramen.
Fig. 1. Schematic view of the gastric wall tear.
After the procedure, artificial ventilation was continued with a Bennett 7200 ventilator until next morning, when the patient was extubated. His circulatory and respiratory functions were normal. Neurological examination revealed no signs of central nervous system lesions. The postoperative period was uneventful, and the patient was discharged home on the eighth postoperative day, in good general condition.
The detailed retrospective analysis did not reveal the precise cause of cardiac arrest in the patient. On the basis of the preoperative examination, smooth and uneventful course of anaesthesia and surgery, as well as highly efficient resuscitation, it can be assumed that cardiac arrest was of a functional (probably reflex) character.
Pneumoperitoneum is a rare complication of resuscitation. In about 10% of resuscitated patients, ventilated without tracheal intubation, autopsy examination reveals superficial tears of gastric mucosa. Most frequently they do not include the full thickness of the gastric wall and cause only minimal to moderate bleeding [2, 3]. The full-thickness gastric wall rupture has so far been described in several cases . In 87% of them the tear was localised at the minor curvature in the subcardial region , possibly because of the diminished elasticity of this part of the stomach wall and its anatomic structure, characterised by scarce mucosal folds [2, 3].
It is currently accepted that gastric rupture is most often the result of a rapid distension by gas. Safar  demonstrated that an "engaged rescuer" is able to fill the stomach with 1900 ml of air, only after several mouth-to-mouth breathes. Most frequently the cause of stomach distension are: high inspiratory pressure, malposition of the mandible and partial airway obstruction. All of these are frequent during ventilation of patients with a laryngeal spasm . Pressure of 15-25 cm H2O (1.5-2.5 kPa) predispose to opening of cardia and filling the stomach with air . Such pressure values are readily possible during mouth-to-mouth or face mask ventilation. At physiological conditions, both the cardia and pylorus act as one way pressure valves. The distension of the stomach, however, changes their anatomical and functional properties, which can make evacuation of gas by the natural route impossible [4, 5].
The pressure needed for full-thickness rupture of the gastric wall has not been precisely established. Krause and Donan , basing on Casenbaum's post-mortem examinations, state that a pressure of 60-120 cm H2O (6-12 kPa) predisposes to a gastric wall rupture at the locus minoris resistentiae i.e. on the minor curvature proximally to the cardia.
External cardiac compression on the lower third of the sternum during resuscitation is an additional factor increasing the intragastric pressure . When the stomach is full, its contents (during compression) may act as a "ram" increasing the pounding force .
In the case presented in this paper, resuscitation was begun by the personnel of the Laryngology Department, before the arrival of the anaesthetic team. Prior to intubation the patient was ventilated mouth-to-mouth, then with a face mask and an AMBU bag. This obviously contributed to the successful reanimation, but could also be the cause of the described complication.
The successful resuscitation cannot determine the prognosis, which is always doubtful. Mortality rate in patients with full-thickness gastric wall rupture during resuscitation is as high as 80% .
The consequences of gastric wall rupture and pneumoperitoneum may be per se life -threatening. The high intraperitoneal pressure displaces the diaphragm upwards diminishing the venous return with untoward haemodynamic consequences [5, 7]. Arterial pressure drop and tachycardia observed in the presented case confirm these observations.
Other risks of gastric wall rupture include bleeding from damaged mucosa and the development of peritonitis, especially when the stomach is full. These complications did not occur in our patient, probably because of the fact that the complication arose in the early postoperative period in a person with an empty stomach.
Originally published in Anestezjologia Intensywna Terapia 31; (3), 195-197, 1999.
1. Pedersen T., Eliasen K., Henriksen E.: A prospective study of risk factors and cardiopilmonary complications associated with anaesthesia and surgery; risk indicators of cardiopulmonary morbidity. Acta Anaesthesiologica Scandinavica 1990, 34, 144-145.
2. Darke S. G., Bloomfiled E.: Case of complete gastric rupture complicating resucitation. British Medical Journal 1975, 16, 414-415.
3. Demos N. J., Poticha S. M.: Gastric rupture occurring during external cardiac rescitation. Surgery 1964, 55, 364-366.
4. Bintz M., FACS, Coghil T. H.: Gastric rupture after the Heimlich maneuver. The Journal of Trauma: Injury, Infection and Critical Care 1996, 40, 159-160.
5. Millata B., Gayral F., Simonneau G., Alasseur F., Larrieu H.: Rupture de l'estomac sain par distension gazeuse. Gastroenterologie Clinique et Biologique 1981, 5, 640-645.
6. Safar P.: Ventilation efficacy of mouth - to - mouth artifical respiration: airway obstruction during manual and mouth - to - mouth artifical respiration. Journal of the American Association 1958, 167, 335-341.
7. Larsen K. M., Laursen R. J.: Repture of the stomach caused by manual ventilation during laryngospasm. Acta Anaesthesiologica Scandinavica 1996, 40, 130-131.
8. Krause S., Donen N.: Gastric repture during cardiopulmonary resusciation. Canadian Anaesthesists Society Journal 1984, 31, 319-322.
9. Linch D., McDonald A., McNicol L.: Tension pneumoperitoneum complicating cardiac resusitation. Intensive Care Medicine 1979, 5, 93-94.