363
Bronchospasm Under Spinal Anaesthesia for Transurethral Resection of Prostate M. ZACHARIAH,· G. KORULAt AND S. NAGAMANI*
Department of Anaesthesia, Christian Medical Col/ege Hospital, Vel/ore, Tamil Nadu, South India
Key Words: ANAESTHETIC TECHNIQUES: spinal; SURGERY: transurethral resection of prostate; COMPLICATIONS: bronchospasm
A 70-year-old man weighing 44 kg, a smoker and asthmatic for 30 years, was scheduled for transurethral resection of the prostate. He was on regular oral Deriphyllin (hydroxyethyl theophylline 77.0 mg and theophylline hydrated 23.0 mg ASTA Pharma, Germany) three times a day for his asthma and his acute attacks had to be treated with subcutaneous adrenaline in the past. He did not give any history of allergy or any other systemic disorder. During routine preoperative examination he looked comfortable in bed, not in obvious respiratory distress. He was afebrile. The only positive finding on general examination was minimal clubbing. Examination of the respiratory system revealed diminished chest expansion. There were bilateral scattered rhonchi and crepitations. Haematocrit was 48%. Chest X-ray showed emphysematous changes and increased bronchovascular markings. Pulmonary function tests showed a vital capacity of 1.1 litres against a predicted value of2.2Iitres, and an FEV 1NC ratio of 50% improved to 55% with bronchodilator, demonstrating severe obstructive and restrictive defects. Deriphyllin was continued and he had regular chest physiotherapy. The patient was premedicated with diazepam 5 mg and Deriphyllin 100 mg orally two hours before surgery. On arrival in the operating room an intravenous infusion was started with Ringers lactate solution. ECG and blood pressure were monitored. A spinal anaesthetic with lignocaine 5% 1 ml (hyperbaric) was performed at the L3-L4 interspace. The upper level of analgesia was at T 10 level at five minutes. He received oxygen at 3 I1min through a Hudson mask. OM. D., D.A., Reader. tM.D., D.A., Associate Professor. *M.D., D.A., Lecturer. Address for Reprints: Dr. M. Zachariah, Department of Anaesthesia, Christian Medical College Hospital, Vellore 6320004, Tamil Nadu, South India. Accepted for publication March 25, 1992 Anaesthesia and Intensive Care. Vol. 10, No. 3. August, 1991
The patient was placed in the lithotomy position and the operation proceeded. The solution used for irrigation was 1.5% glycine suspended from a height of 50 cm. Blood pressure and pulse were stable during the first twenty minutes of the procedure. The patient was breathing comfortably and was talking till this time. Then he complained of difficulty in breathing. On auscultation, there were rhonchi over both lungfields. Deriphyllin 100 mg was given intravenously without response. He then became apnoeic, developed bradycardia and asystolic cardiac arrest. He was intubated with a 9 mm cuffed endotracheal tube and IPPV was commenced with 100% oxygen. Inflation pressure was felt to be very high. He also received atropine 0.6 mg and adrenaline 1:10,000 5 mI. Cardiac massage was started simultaneously. Within a minute, the ECG showed sinus rhythm with a rate of 100/min and the systolic blood pressure was 180 mmHg. This gradually settled down to 120-130 mmHg. The required inflation pressure improved over a period often minutes and the patient started to make attempts at spontaneous breathing. A pulse oximeter was connected at this stage and showed a saturation of 90%. Since bronchospasm persisted, a mixture of 1% halothane and 50% nitrous oxide were added. A bolus dose of 200 mg aminophylline was given and an infusion at a rate of 0.5 mglkg/hr was started. Blood gas analysis at this time showed pH 7.16, PC02 81 mmHg, P02 287 mmHg, HC0 3 28 mEq/l, BE - 3.2 and calculated oxygen saturation 99.6%. Ventilation was assisted to reduce the PC02 to acceptable levels. The blood pressure slowly dropped to 80 mmHg. Aminophylline infusion was replaced with adrenaline at a rate of 0.5 micrograms/kglmin. Blood pressure increased to 110-120 mmHg. Heart rate stayed at 120/min. The surgeon was allowed to proceed with haemostasis. The lungs became clearer and the patient was extubated at the end of the surgery when he responded to commands and was breathing adequately.
364
M. ZACHARIAH ET AL
After extubation he was allowed to breathe 100% oxygen from the circle absorber circuit. Gradually he became drowsy and did not respond to commands even though the pulse oximeter read 94-95%. The F i o 2 was reduced to 30% by supplementing with 2 l/min of oxygen through an Ambu resuscitator Mark III without a reservoir bag. The patient became more alert and awake. Serum biochemistry showed N a + 127 mEq/l, K + 3.6 mEq/l. Haematocrit was 42%. He was transferred to the intensive care unit for further management where he continued to have mild bronchospasm. Salbutamol 2.5 mg was given through a nebuliser. Adrenaline infusion was replaced with terbutaline 2.5 mg over eight hours. Twenty-eight per cent oxygen was administered through a venturi mask. The bronchospasm eased slowly over the next six hours. Arterial blood gas analysis the next day showed pH 7.358, PC02 56 mmHg, P02 76 mmHg, HC03 30.9 mEq/l, BE - 4.0, oxygen saturation 93.4%. The patient was stablised on oral Deriphyllin and salbutamol and was discharged from hospital a week later. DISCUSSION
We chose to give spinal anaesthesia to this patient for two reasons. (1) In patients undergoing transurethral resection of prostate early signs of intravascular absorption of irrigating fluid or accidental urinary bladder perforation can be detected early in awake patients. I (2) In asthmatic patients regional anaesthesia is often the preferred anaesthetic option for surgery on the extremities and for urological procedures. This avoids intubation which is the one factor that has been shown to precipitate bronchospasm in patients with hyper-reactive airways, if reflexes are not suppressed. However, regional anaesthesia does not guarantee protection from bronchospasm. McGough and Cohen have reported a case with severe bronchospasm during spinal anaesthesia. 2 In a study by Schnider and Papper, 6.4% of asthmatics developed wheezing during general anaesthesia following intubation, whereas less than 2% did so with either general anaesthesia without intubation or with regional anaesthesia. 3 Psychological factors can interact with the asthmatic diathesis to reduce airway calibre. 4 Fear and anxiety may have been the precipitating factor in this patient. Better sedation may have prevented this. Moreover, people living in tropical countries such as ours are used to a warm environment. Sudden exposure to a cold operating room may also have contributed. High sympathetic block could lead to bronchospasm by vagal overactivity. The cardiovascular effects of a 'central' sympathetic block (Tl-T 4) are decreased cardiac output and sudden bradycardia. 5 This patient did not have any
hypotension or bradycardia before the bronchospasm to suggest a high sympathetic block and vagal preponderance. Cardiac arrest in this patient, we feel, was due to severe hypoxia from bronchospasm. The adrenaline and atropine in addition to restoring cardiac function would have relaxed the bronchial musculature. The high airway pressures required for ventilation gradually came down with this treatment. Even though intubation is better avoided in asthmatics, once severe bronchospasm occurs, intubation and IPPV may become mandatory for optimising gas exchange. Another possible cause for bronchospasm under spinal anaesthesia is allergic reaction to the local anaesthetic. Among the local anaesthetics, aminoesters are more liable to produce allergic reactions than aminoamides. These patients develop generalised flushing with wheals, facial swelling and respiratory distress within ten minutes of injection. 6 ,7 Our patient developed bronchospasm 20 minutes after the spinal anaesthetic and did not have any of the associated symptoms described above. TURP syndrome from absorption of irrigation fluid is a possible consideration in this patient. However, we feel it is unlikely for the following reasons. There was no clinical evidence of circulatory overloading such as fine crepitations or raised jugular venous pressure. The CVP was 9 cm of H 20. He had received only 300 ml of Ringer's solution till the time of arrest. We did not have to use diuretics during or after surgery. The serum sodium and potassium were within acceptable limits. There was no anaemia. Even though transurethral resection of the prostate syndrome may occur within a short period of resection, most of the case reports have been after prolonged resection time. 8 In our patient, the bronchospasm occurred after resecting 109 of an estimated 40 g of prostatic tissue. The fact that some patients with chronic obstructive pulmonary disease are dependent on hypoxic drive is brought home in this report. After being awake at the end of surgery, the patient became drowsy on inhaling 100% 02. In our enthusiasm to improve the oxygen saturation we overlooked the fact that this patient could have been dependent on hypoxic drive for maintenance of alveolar ventilation. The lowest F i o 2 necessary to keep the oxygen saturation within acceptable limits should be chosen to avoid hypoventilation.
REFERENCES
1. Stoelting RK, Dierdorf SF, McCammon RL. Anaesthesia and Co-existing Disease. 2nd Edition Churchill Livingstone 1988; 441. Anaesthesia and IntensIve Care, Vol 20, No. 3, August, 1992
CASE REPORT 2. McGough EK, Cohen JA. Unexpected bronchospasm during spinal anaesthesia. J Clin Anesth 1990; 2,1:35-36. 3. Shnider SM, Papper EM. Anaesthesia for the asthmatic patient. Anesthesiology 1961; 22:886-892. 4. Harrison's Principles ofInternal Medicine. 12th Ed, McGraw-Hill, Inc 1991; Vo12; 1049. 5. Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anaesthesia and Management of Pain. 2nd Ed, J. B. Lippincott Company, Philadelphia 1987; 279.
365
6. Brown DT, Beamish D, Wildsmith J. Allergic reactions to an amide local anaesthetic. Br J Anaesth 1981; 53: 435. 7. Fisher MM, Pennington Pc. Allergy to local anaesthesia. Br J Anaesth 1982; 54:893. 8. Norris HT, Aasheim GM, Sherrard DJ, Tremann JA. Symptomatology Pathophysiology and Treatment of the Transurethral Resection of the Prostate Syndrome. Br J Urol 1973; 45:420-427.
Post Partum Airway Obstruction After Vaginal Delivery R. J. EBERT*
Department of Anaesthetics, Faculty of Medicine, University of Natal, Durban, South Africa
Key Words: OBSTETRICS: acute laryngeal oedema, pre-eclamptic toxaemia
Laryngeal oedema is a rare condition in pregnancy. The diagnosis is frequently made at laryngoscopy for caesarean section, and may make intubation and extubation of the trachea difficult. This patient, with pregnancy-induced hypertension, developed acute airways obstruction requiring intubation eight hours after vaginal delivery, a situation not previously reported. CASE REPORT A 23-year-old African woman was referred to the Obstetric Unit at King Edward VIII Hospital, Durban, complaining of headache, abdominal pains and swelling of the limbs for the past week. She was unsure of her dates but was thought to be about 24 weeks pregnant. Blood pressure recorded by the referring doctor was 1901130 mmHg. She had no previous medical or obstetric history. On admission she was noted to be puffy, with bipedal oedema and brisk reflexes. Her blood pressure was 240/140 mmHg, with no signs of cardiomegaly. Abdominal and ultrasound examination confirmed the presence of an approximately 29-week fetus with an estimated weight of 1.0 kg. She was not weighed on admission, but her post delivery weight was 53 kg and her height 1.47 metres. Investigations showed a haemoglobin of 10 gld!. Renal and coagulation profiles were normal apart *F.F.A.R.A.C.S., B.Se. (Cantab.), Anaesthetist. Address for Reprints: Dr. R. J. Ebert, Department of Anaesthesia, Christehureh Hospital, Private Bag 4710, Christehureh, New Zealand. Accepted for publication March 25, 1992 Anaesthesia and Intensive Care, Vot 20, No. 3, August, 1992
from a uric acid level of 0.46 mmol/litre, an elevated level for the period of gestation. The urine was repeatedly blood stained, making protein estimation unreliable. The diagnosis was one of severe hypertensive crisis of pregnancy. Conservative management was decided upon initially in an attempt to improve fetal outcome. Initial control of blood pressure was achieved with phenobarbitone 200 mg intramuscularly and nifedipine 10 mg sublingually. She was started on aldomet 500 mg six-hourly and aspirin 75 mg daily. Hydrallazine 50 mg six-hourly was subsequently added to her anti-hypertensive regime. She received dexamethasone 8 mg eight-hourly to aid fetal lung maturation. Forty-eight hours later she required transfer to the Labour Ward for further control of her blood pressure which had spiked to 200/120 mmHg. The patient was advised to have the pregnancy terminated. She was commenced on a magnesium sulphate regimen, consisting of 4 g slowly intravenously, 5 g intramuscularly in each buttock, and 5 g intramuscularly four-hourly. Blood pressure peaks were controlled with nifedipine 10 mg sublingually on two occasions. Labour was induced with the aid of extra-amniotic prostaglandin (F2alpha) infusion, rupture of membranes and oxytocin. After three-and-a-half hours of labour she had a breach delivery of a 1.1 kg live male infant. The placenta appeared complete with an estimated blood loss at delivery of 100 m!.
Bronchospasm Under Spinal Anaesthesia for Transurethral Resection of Prostate M. ZACHARIAH,· G. KORULAt AND S. NAGAMANI*
Department of Anaesthesia, Christian Medical Col/ege Hospital, Vel/ore, Tamil Nadu, South India
Key Words: ANAESTHETIC TECHNIQUES: spinal; SURGERY: transurethral resection of prostate; COMPLICATIONS: bronchospasm
A 70-year-old man weighing 44 kg, a smoker and asthmatic for 30 years, was scheduled for transurethral resection of the prostate. He was on regular oral Deriphyllin (hydroxyethyl theophylline 77.0 mg and theophylline hydrated 23.0 mg ASTA Pharma, Germany) three times a day for his asthma and his acute attacks had to be treated with subcutaneous adrenaline in the past. He did not give any history of allergy or any other systemic disorder. During routine preoperative examination he looked comfortable in bed, not in obvious respiratory distress. He was afebrile. The only positive finding on general examination was minimal clubbing. Examination of the respiratory system revealed diminished chest expansion. There were bilateral scattered rhonchi and crepitations. Haematocrit was 48%. Chest X-ray showed emphysematous changes and increased bronchovascular markings. Pulmonary function tests showed a vital capacity of 1.1 litres against a predicted value of2.2Iitres, and an FEV 1NC ratio of 50% improved to 55% with bronchodilator, demonstrating severe obstructive and restrictive defects. Deriphyllin was continued and he had regular chest physiotherapy. The patient was premedicated with diazepam 5 mg and Deriphyllin 100 mg orally two hours before surgery. On arrival in the operating room an intravenous infusion was started with Ringers lactate solution. ECG and blood pressure were monitored. A spinal anaesthetic with lignocaine 5% 1 ml (hyperbaric) was performed at the L3-L4 interspace. The upper level of analgesia was at T 10 level at five minutes. He received oxygen at 3 I1min through a Hudson mask. OM. D., D.A., Reader. tM.D., D.A., Associate Professor. *M.D., D.A., Lecturer. Address for Reprints: Dr. M. Zachariah, Department of Anaesthesia, Christian Medical College Hospital, Vellore 6320004, Tamil Nadu, South India. Accepted for publication March 25, 1992 Anaesthesia and Intensive Care. Vol. 10, No. 3. August, 1991
The patient was placed in the lithotomy position and the operation proceeded. The solution used for irrigation was 1.5% glycine suspended from a height of 50 cm. Blood pressure and pulse were stable during the first twenty minutes of the procedure. The patient was breathing comfortably and was talking till this time. Then he complained of difficulty in breathing. On auscultation, there were rhonchi over both lungfields. Deriphyllin 100 mg was given intravenously without response. He then became apnoeic, developed bradycardia and asystolic cardiac arrest. He was intubated with a 9 mm cuffed endotracheal tube and IPPV was commenced with 100% oxygen. Inflation pressure was felt to be very high. He also received atropine 0.6 mg and adrenaline 1:10,000 5 mI. Cardiac massage was started simultaneously. Within a minute, the ECG showed sinus rhythm with a rate of 100/min and the systolic blood pressure was 180 mmHg. This gradually settled down to 120-130 mmHg. The required inflation pressure improved over a period often minutes and the patient started to make attempts at spontaneous breathing. A pulse oximeter was connected at this stage and showed a saturation of 90%. Since bronchospasm persisted, a mixture of 1% halothane and 50% nitrous oxide were added. A bolus dose of 200 mg aminophylline was given and an infusion at a rate of 0.5 mglkg/hr was started. Blood gas analysis at this time showed pH 7.16, PC02 81 mmHg, P02 287 mmHg, HC0 3 28 mEq/l, BE - 3.2 and calculated oxygen saturation 99.6%. Ventilation was assisted to reduce the PC02 to acceptable levels. The blood pressure slowly dropped to 80 mmHg. Aminophylline infusion was replaced with adrenaline at a rate of 0.5 micrograms/kglmin. Blood pressure increased to 110-120 mmHg. Heart rate stayed at 120/min. The surgeon was allowed to proceed with haemostasis. The lungs became clearer and the patient was extubated at the end of the surgery when he responded to commands and was breathing adequately.
364
M. ZACHARIAH ET AL
After extubation he was allowed to breathe 100% oxygen from the circle absorber circuit. Gradually he became drowsy and did not respond to commands even though the pulse oximeter read 94-95%. The F i o 2 was reduced to 30% by supplementing with 2 l/min of oxygen through an Ambu resuscitator Mark III without a reservoir bag. The patient became more alert and awake. Serum biochemistry showed N a + 127 mEq/l, K + 3.6 mEq/l. Haematocrit was 42%. He was transferred to the intensive care unit for further management where he continued to have mild bronchospasm. Salbutamol 2.5 mg was given through a nebuliser. Adrenaline infusion was replaced with terbutaline 2.5 mg over eight hours. Twenty-eight per cent oxygen was administered through a venturi mask. The bronchospasm eased slowly over the next six hours. Arterial blood gas analysis the next day showed pH 7.358, PC02 56 mmHg, P02 76 mmHg, HC03 30.9 mEq/l, BE - 4.0, oxygen saturation 93.4%. The patient was stablised on oral Deriphyllin and salbutamol and was discharged from hospital a week later. DISCUSSION
We chose to give spinal anaesthesia to this patient for two reasons. (1) In patients undergoing transurethral resection of prostate early signs of intravascular absorption of irrigating fluid or accidental urinary bladder perforation can be detected early in awake patients. I (2) In asthmatic patients regional anaesthesia is often the preferred anaesthetic option for surgery on the extremities and for urological procedures. This avoids intubation which is the one factor that has been shown to precipitate bronchospasm in patients with hyper-reactive airways, if reflexes are not suppressed. However, regional anaesthesia does not guarantee protection from bronchospasm. McGough and Cohen have reported a case with severe bronchospasm during spinal anaesthesia. 2 In a study by Schnider and Papper, 6.4% of asthmatics developed wheezing during general anaesthesia following intubation, whereas less than 2% did so with either general anaesthesia without intubation or with regional anaesthesia. 3 Psychological factors can interact with the asthmatic diathesis to reduce airway calibre. 4 Fear and anxiety may have been the precipitating factor in this patient. Better sedation may have prevented this. Moreover, people living in tropical countries such as ours are used to a warm environment. Sudden exposure to a cold operating room may also have contributed. High sympathetic block could lead to bronchospasm by vagal overactivity. The cardiovascular effects of a 'central' sympathetic block (Tl-T 4) are decreased cardiac output and sudden bradycardia. 5 This patient did not have any
hypotension or bradycardia before the bronchospasm to suggest a high sympathetic block and vagal preponderance. Cardiac arrest in this patient, we feel, was due to severe hypoxia from bronchospasm. The adrenaline and atropine in addition to restoring cardiac function would have relaxed the bronchial musculature. The high airway pressures required for ventilation gradually came down with this treatment. Even though intubation is better avoided in asthmatics, once severe bronchospasm occurs, intubation and IPPV may become mandatory for optimising gas exchange. Another possible cause for bronchospasm under spinal anaesthesia is allergic reaction to the local anaesthetic. Among the local anaesthetics, aminoesters are more liable to produce allergic reactions than aminoamides. These patients develop generalised flushing with wheals, facial swelling and respiratory distress within ten minutes of injection. 6 ,7 Our patient developed bronchospasm 20 minutes after the spinal anaesthetic and did not have any of the associated symptoms described above. TURP syndrome from absorption of irrigation fluid is a possible consideration in this patient. However, we feel it is unlikely for the following reasons. There was no clinical evidence of circulatory overloading such as fine crepitations or raised jugular venous pressure. The CVP was 9 cm of H 20. He had received only 300 ml of Ringer's solution till the time of arrest. We did not have to use diuretics during or after surgery. The serum sodium and potassium were within acceptable limits. There was no anaemia. Even though transurethral resection of the prostate syndrome may occur within a short period of resection, most of the case reports have been after prolonged resection time. 8 In our patient, the bronchospasm occurred after resecting 109 of an estimated 40 g of prostatic tissue. The fact that some patients with chronic obstructive pulmonary disease are dependent on hypoxic drive is brought home in this report. After being awake at the end of surgery, the patient became drowsy on inhaling 100% 02. In our enthusiasm to improve the oxygen saturation we overlooked the fact that this patient could have been dependent on hypoxic drive for maintenance of alveolar ventilation. The lowest F i o 2 necessary to keep the oxygen saturation within acceptable limits should be chosen to avoid hypoventilation.
REFERENCES
1. Stoelting RK, Dierdorf SF, McCammon RL. Anaesthesia and Co-existing Disease. 2nd Edition Churchill Livingstone 1988; 441. Anaesthesia and IntensIve Care, Vol 20, No. 3, August, 1992
CASE REPORT 2. McGough EK, Cohen JA. Unexpected bronchospasm during spinal anaesthesia. J Clin Anesth 1990; 2,1:35-36. 3. Shnider SM, Papper EM. Anaesthesia for the asthmatic patient. Anesthesiology 1961; 22:886-892. 4. Harrison's Principles ofInternal Medicine. 12th Ed, McGraw-Hill, Inc 1991; Vo12; 1049. 5. Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anaesthesia and Management of Pain. 2nd Ed, J. B. Lippincott Company, Philadelphia 1987; 279.
365
6. Brown DT, Beamish D, Wildsmith J. Allergic reactions to an amide local anaesthetic. Br J Anaesth 1981; 53: 435. 7. Fisher MM, Pennington Pc. Allergy to local anaesthesia. Br J Anaesth 1982; 54:893. 8. Norris HT, Aasheim GM, Sherrard DJ, Tremann JA. Symptomatology Pathophysiology and Treatment of the Transurethral Resection of the Prostate Syndrome. Br J Urol 1973; 45:420-427.
Post Partum Airway Obstruction After Vaginal Delivery R. J. EBERT*
Department of Anaesthetics, Faculty of Medicine, University of Natal, Durban, South Africa
Key Words: OBSTETRICS: acute laryngeal oedema, pre-eclamptic toxaemia
Laryngeal oedema is a rare condition in pregnancy. The diagnosis is frequently made at laryngoscopy for caesarean section, and may make intubation and extubation of the trachea difficult. This patient, with pregnancy-induced hypertension, developed acute airways obstruction requiring intubation eight hours after vaginal delivery, a situation not previously reported. CASE REPORT A 23-year-old African woman was referred to the Obstetric Unit at King Edward VIII Hospital, Durban, complaining of headache, abdominal pains and swelling of the limbs for the past week. She was unsure of her dates but was thought to be about 24 weeks pregnant. Blood pressure recorded by the referring doctor was 1901130 mmHg. She had no previous medical or obstetric history. On admission she was noted to be puffy, with bipedal oedema and brisk reflexes. Her blood pressure was 240/140 mmHg, with no signs of cardiomegaly. Abdominal and ultrasound examination confirmed the presence of an approximately 29-week fetus with an estimated weight of 1.0 kg. She was not weighed on admission, but her post delivery weight was 53 kg and her height 1.47 metres. Investigations showed a haemoglobin of 10 gld!. Renal and coagulation profiles were normal apart *F.F.A.R.A.C.S., B.Se. (Cantab.), Anaesthetist. Address for Reprints: Dr. R. J. Ebert, Department of Anaesthesia, Christehureh Hospital, Private Bag 4710, Christehureh, New Zealand. Accepted for publication March 25, 1992 Anaesthesia and Intensive Care, Vot 20, No. 3, August, 1992
from a uric acid level of 0.46 mmol/litre, an elevated level for the period of gestation. The urine was repeatedly blood stained, making protein estimation unreliable. The diagnosis was one of severe hypertensive crisis of pregnancy. Conservative management was decided upon initially in an attempt to improve fetal outcome. Initial control of blood pressure was achieved with phenobarbitone 200 mg intramuscularly and nifedipine 10 mg sublingually. She was started on aldomet 500 mg six-hourly and aspirin 75 mg daily. Hydrallazine 50 mg six-hourly was subsequently added to her anti-hypertensive regime. She received dexamethasone 8 mg eight-hourly to aid fetal lung maturation. Forty-eight hours later she required transfer to the Labour Ward for further control of her blood pressure which had spiked to 200/120 mmHg. The patient was advised to have the pregnancy terminated. She was commenced on a magnesium sulphate regimen, consisting of 4 g slowly intravenously, 5 g intramuscularly in each buttock, and 5 g intramuscularly four-hourly. Blood pressure peaks were controlled with nifedipine 10 mg sublingually on two occasions. Labour was induced with the aid of extra-amniotic prostaglandin (F2alpha) infusion, rupture of membranes and oxytocin. After three-and-a-half hours of labour she had a breach delivery of a 1.1 kg live male infant. The placenta appeared complete with an estimated blood loss at delivery of 100 m!.
