Naeem A. Zubair ( Departments of Anaesthesia, The Aga Khan University Hospital, Karachi. )
Farah Saleem ( Departments of Obstetrics and Gynaecology, The Aga Khan University Hospital, Karachi. )
Nadeem Zaidi ( Departments of Anaesthesia, The Aga Khan University Hospital, Karachi. )
Zeenat E. Kban ( Departments of Anaesthesia, The Aga Khan University Hospital, Karachi. )
Ursula Chohan ( Departments of Anaesthesia, The Aga Khan University Hospital, Karachi. )
February 1998, Volume 48, Issue 2
Case Reports
Introduction
Spinal anaesthesia is associated with certain complications such as severe hypotension, post-spinal headache, meningitis, audio- visual disturbances and some time transient or permanent neurological damage. Now-a-days spinal anaesthesia is in demand again due to cost effectiveness, rapidity and predictability of effects1 and decreased rate of complications2. A case of a young woman who received spinal analgesia for labor and within twenty-four hours, developed a throbbing heathche is reported here.
On the fourth post-spinal day she complained of visual disturbances which rapidly led to complete blindness. The problem of an appropriate diagnosis of the cause could lead to medicolegal issues.
Case Report
A healthy primigravida (P0+0, G-1) 26 years of age who is a nurse by profession was admitted to the maternity unit at Aga Khan University Hospital for elective induction of labor. Atthetime ofadmissionshe hadhistoiy ofamnenorrhea for40+ weeks. She was a registered case at the antenatal clinic where she made thirteen visits before her final admission for elective induction of labor. The antenatal course was uneventful except one admission due to lowerabdominal pain. On the day of admission for induction of labor she was well orientated in time and space. The physical and laboratoiy examinations were within normal limits. Shewas not in active labor. The vaginal examination revealed cervical dilatation of 1.5 cm, cephalic presentation and intact membranes. Tablet prostin (PG £2) was inserted and two hours later artificial rupture of membranes (ARM) was done. A continuous infusion of syntocinon (10 I.U. in 500 ml 5% D/W) was started. Analgesia was provided with injections of pethidine/promethazine 75 mg/25 mg intramuscularly. With the progress of labor the pain became unbearable. She was very restless, uncooperative and unmanageable. Vaginal examination showed a cervical dilatation of 6+ cm. Regional analgesia was offered and was accepted by the patient. Spinal route was chosen because a rapid, reliable and effective pain relief was needed and it was also estimated that she will deliver within next two to two and a half hours. The patient was informed aboyt the procedure and a verbal consent was obtained. She was preloaded with 750 ml of ringer lactate fluid. Using the standard precautions of aseptic technique and proper preparation of the skin, intrathecal space was entered at the level of L3-L4 with 22 gauge spinal needle and entry was confirmed with the free flow of clear CSF. Isobaric Marcaine 0.5% 2.5 ml (12.5 mg) was injected intrathecally with the patient in sitting position. Soon a block upto T8-T9 was established and the patient had instant pain relief Her vital signs did not change significantly. A healthy baby with apgar score of 9/10 was delivered spontaneously through vaginal route under spinal analgesia. Within twenty four hours of spinal analgesia the patient complained of headache, that was throbbing in nature and was located in the tempom-frontal region but poorly related to the posture. The physical examination showed no signs of meningeal irritation. A provisional diagnosis of post-spinal headache was made and conservative treatment with NSAID, hydration and bed rest was started. The conservative management did not give any significant relief to her complaint Cafergot (Caffeine plus ergotamine) orally was added to the regime over the next twenty-four hours and even injection pethidine was given on PRN bases to manage her problem. On the third post-partum day the patient continued to have headache and the possibility ofanepiduralbloodpatchwasdiscussed. Thevital signs’ chart showed a consistently elevated blood pressure (140-150/100-110 mmHg) over the last twenty-four hours. By this time the patient was a bit confused and neurotic. A consultation from a psychiatrist was requested, On the morning of the fourth post-partum thy she still had severe headache and also developed blurring of vision. Within the next few hours the patient complained of complete blindness. At that time herphysical examination showed abloodpressure of 180/90 mmHg, mild neck rigidity, while ophthalmoscopic examination showed no signs of raised intracranial pressure.
A consultation from a neurologist was asked and a CT scan of the brain was advised. The CT scan showed diffuse cerebrM edema, meningeal enhancement with no-mid line shift. All hematological tests were within normal limits except raised LDH level (LDH 778 u/ml). The CSF sample was obtained for detailed examination and culture/sensitivity. It was blood stained and the examination revealed RBCs, high protein levelá and lymphocytes 95% (Glucose 60 mg/dl, chloride 124 mmol/l, protein 269 mg/dl, TLC 88/mi lymphocytes 95%). RBCs 8912/nil, CSF Culture: Few colonies of staphylococcus species. A provisional diagnosis of meningitis (viral or bacterial) or pm- eclampsia/eclampsia was made and treatment started with antibiotics, anti-hypertensive drugs and mannitol. The patient was transferred to ICU for further management The MIRI study on the next thy, showed evidence of high signal, minimal subdural fluid collection over both cerebral hemispheres and left cerebellar hemisphere. There were also areas of abnormal signal intensity inboth occipital lobes in the deep white matter of the brain in the parietal region and in the cerebellar hemispheres. These findings are suggestive of areas of infarct which could be attributed to vasculitis, meningitis or cerebral oedema. The patient was still very restless, confused and blind. Decadrone was added to the therapy. An elective intubation and mild hyperventilation was planned but was not instituted. On sixth post-partum thy the clinical condition improved and she started recognizing people. Her blood pressure returned to normal limits (125/75 nmHg). Another sample of CSF was drawn and sent for examination which showed normal protein level and almost non- significant numbers ofRBCs (Glucose 61 mg/dl, Chloride 126 mmol/l, protein 33 mgfdl, TLC 4/nil, RBCs 80/nil). CSF culture examination revealed no bacterial growth. Her eye sight gradually improved over the next three days. She made an uneventful recovery and was discharged home with normal ocular acuity and normal blood pressure. Another MRI study was done three weeks later to the first study, which showed completed resolution of previous abnormal findings. There were no further complaints in her post-natal follow-up.
Discussion
Spinal anaesthesia is favoured because of rapidity of onset of action and reliability. Technically it is easy to perform and is associated with fewer complications1 . Post spinal heathche is one of the known complication and in majority of the patients it develops within 2448 hours. It involves mainly the occipital and frontal areas and gets worse with change of posture but a group of patients might have post3spinal headache with poor correlation to posture4. The headache is due to slow leak of CSF which leads to contraction of subarachnoid space and compensatory expansion of the pain sensitive intracranial veins5. Itcanbe associated with auditory and vestibular symptoms6. The incidence of heathche has decreased since the use of special .pnd fine needles7 such as Quincke needles or Sprotte needles and even in Obstetrics it is only 1.6% with 22 or24 gauge Sprotte needles8. In majority of the cases it resolves completely within 5 days (1-12 days) with conservative treatment but a few may need autologous epidural blood patch6 . In younger age group of patients postspinal headache could be due to other reasons2 and when headache persists despite conservative treatment, the patient should bc carefully evaluated for any other associated pathology9 . In this patient typical post-spinal headache started within twenty -four hours after delivery and was poorly related to posture. Her symptoms were not relieved with conservative treatment and invasive management with epidural blood patch was withheld with the view that it would settle down within few days. Associated symptoms such as auditgry and vest ibular are seen with moderate to severe headache6 . Ocular symptoms such as double vision, blurring, inability to read and abducens palsy have also been documented10 but blindness has never been reported which occurred in this patient. The sudden changes in the intracranial pressure due to CSF leak, compensatory dilatation and traction of intracranial vessels could result in tearing of these vessels and haemorrhage. Haemorrhage in the cortical area can lead to blindness. When blindness is of cortical origin, it is characterized by intact pupillary light reflex and normal ophthalmoscopic findings11 and these findings were present in this patient. In cortical blindness, altered state of consciousness is seen and is due to the lesions in the deeper white matter or basal ganglia12. This patient did have altered mental status and lesions in the deeper white matter. The persistently elevated blood pressure since the postpartum period, findings of CT scan of brain, CSF examination andMRI study results, changedthe diagnosis and she was treated as a case of meningitis or severe pre-eclampsia. During pregnancy induced hypertension the cerebral blood velocity and resistance to flow is increased due to vascular changes. Velocity and resistance increases even more in immediate puerperal period. A transient alteration in the blood brain barner and increased intracellular fluid secondary to transient cellular ischaernia is also seen in patients with preeclamptic toxemia. These changes could lead to cerebral edema and petichial haemorrhages with consequent focal neurological lesions and transient cortical blindness in Preeclamptic patients13 . In a retrospective study Cunningham et al11 have shown that majority of the patients with preeclampsia had predominant symptoms of severe headache before the onset of blindness. Similarly in this case severe headache was followed by blindness. The reported duration of blihdness ranges from four hours to 192 hours ( eight days?, in different patients, although it resolves completely . This patient started recognizing people after forty-eight hours of blindness and recovered fully in six to seven days. The case reported here raises interesting and important questions about diagnosis and management. Did she really have a post-spinal headache or was the headache an early sign of pre-eclampsia? She had a typical post-spinal headache within first twenty four hours, this could be due to the use of 22 gauge needle, as the incidence of headache is higher with wide bore spinal needles. It is also difficult to rule out that cerebral changes were not there before spinal anaesthesia was established. She was treated conservatively which is a normal practice, as headache in majority of these patients resolves completely with such treatment. Also the application of epidural blood patch could have complicated her clinical condition, rather than benefiting the patient as the pathology was different. The course of events, physical and laboratory findings (raised blood pressure, elevated LDH), CT Scan of brain and MRI study results and the resolution of blindness shows that the cause of the problem was probably underlyign obstetrical pathology rather than spinal analgesia. Spinal analgesia might have contributed to the earlier occurrence of her symptoms. The coincidental combination of spinal analgesia in a patient with underlying obstetrical pathology can lead to misdiagnosis and medicolegal problems.
The lesson to learn from this case is that patient’s complaints should always be taken seriously and investigated properly. The patient should not be treated blindly. A thorough physical examination, proper monitoring of vital signs, neurological assessment and a careful search for other pathology should be made lithe headache persists after spinal anaesthesia especially in obstetric patients.
References
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2. Flaatten, H., Rodt. S,A., Vamncs, J. et at. Postdural puncture headache. A comparison between 26 and 29 gauge needles in young patients. Anesthesia, 1989;44:147-149.
3. Wiesel, S., Tessler, MJ. and Easdown, L.J. Postdural puncture headache: A randomized comparison of the 24 gauge sprotte and the 27 gauge Quincke needles in young patients. Can. 3. Anaesth., 1993;40:607-611.
4. Corbey. M.P., Berg. P. and Quaynor, H. Classification and severity of postdural puncture headache. Comparison of 26 gauge and 27 gauge quincke needle for spinal anaesthesia in day care surgery in patients under 45 years. Anaesthesia, 1993;48:776-781.
5. Morewood, G.H. A rational approach to the cause, prevention and treatment of postdural headache (review). Can. Med. Assoc. J., 1993; 149:1087-1093.
6. Lybecker, H., Djemes, M. and Schmidt, iF. Postdural puncture headache (PDPH): onset, duration, severity and associated symptoms. An analysis of 75 consecutive patients with PDPH. Acta Anaesthesiol. Scand., 1 995;39:605-6 12.
7. Lynch, J., Ka6sper, S.M., Stick, K. et al. The use of Quincke and Whitacre 27-gauge needles in orthopedic patients: Incidence of failed spinal anesthesia and postdural puncture headache. Anesth. Analg., 1994:79:124-128.
8. Sear, D.H.,Leeman, M.l., Jassy, L.J. et al. The frequency of postdural puncture headache in obstetric patients. A prospective study comparing the 24 gauge versus the 22-gauge sprotte needle. J. Clin. Anaesthesia, I 994;6:42-46.
9. Dutton, D.A. A ‘Postspinal headache’ associated with incidental intracranial pathology. Case report. Anaesthesia, 1991 ;46: 1044- 1046.
10. Vandam, L.D. and Dripps, RD. Exacerebration of pre-existing neurologic disease alter spinal anaesthesia. N. EngI. J. Med., 1 956;255 :843-848.
11. Cunningham. F.G., Fernandez, CO. and Hemandez, C. Blindness associated with preeclampsia and eclampsia. Am. 1. Obstet. Gynecol., 1995;172:1291¬1298.
12. Timothy, G., Sanders, S., Clayman, D.A. et al. Brain in eclampsia: MR imaging with clinical correlation. Radiology, 1991 1 80.175-178.
13. Williams, K.P. and Mcleans, C. Peripartum changes in maternal cerebral blood flow velocity in normotensive and preeclamptic patients. Obstet. Gynecol., 1993,82:334-337.
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