|Year : 2008 | Volume
| Issue : 5 | Page : 592
Adverse Outcome in a Patient with Undiagnosed and Asymptomatic Intracranial Lesion after Total Abdominal Hysterectomy
Anurag Tewari1, Shuchita Garg2, Atul Mishra3, Dinesh Sood4, Chiteshwar Walia5, Tej K Kaul6
1 Assistant Professor, Anaesthesiology, Dayanand Medical College & Hospital, Ludhiana, Punjab, India
2 Senior Consultant, Intensive Care, Dayanand Medical College & Hospital, Ludhiana, Punjab, India
3 Associate Professor, Surgery, Dayanand Medical College & Hospital, Ludhiana, Punjab, India
4 Professor, Anaesthesiology, Dayanand Medical College & Hospital, Ludhiana, Punjab, India
5 Senior Resident, Anaesthesiology, Dayanand Medical College & Hospital, Ludhiana, Punjab, India
6 Professor & Head, Professor & Head, Anaesthesiology Dayanand Medical College & Hospital, Ludhiana, Punjab, India
|Date of Acceptance||20-Jul-2008|
|Date of Web Publication||19-Mar-2010|
126-D, Kitchlu Nagar, Ludhiana, Punjab,141001
Source of Support: None, Conflict of Interest: None
We describe a case of 55-year-old female who had deterioration of respiratory and haemodynamic status after hysterectomy under subarachnoid block. On the second postoperative day she had to be intubated and sustained on ventilatory and inotropic support. The patient had apparently no previous cardio-respiratory-renal or neurological problem. Her CT scan revealed a space occupying intracranial lesion. The etiopathogensis and future management of such patients is discussed after review of current literature.
Keywords: Subarachnoid blockade, intracranial lesion.
|How to cite this article:|
Tewari A, Garg S, Mishra A, Sood D, Walia C, Kaul TK. Adverse Outcome in a Patient with Undiagnosed and Asymptomatic Intracranial Lesion after Total Abdominal Hysterectomy. Indian J Anaesth 2008;52:592
|How to cite this URL:|
Tewari A, Garg S, Mishra A, Sood D, Walia C, Kaul TK. Adverse Outcome in a Patient with Undiagnosed and Asymptomatic Intracranial Lesion after Total Abdominal Hysterectomy. Indian J Anaesth [serial online] 2008 [cited 2020 Oct 24];52:592. Available from: https://www.ijaweb.org/text.asp?2008/52/5/592/60683
| Introduction|| |
Several anaesthetic techniques have been described for total abdominal hysterectomy and most frequently spinal anaesthesia is used for these surgeries. Although a safe procedure, it can be associated with neurological complications like post dural puncture headache, transient neurological disturbances, seizures and rarely radiculopathy and myelopathy , . Diagnosis of a brain tumour after spinal anaesthesia is rare  ; however, a few cases have been mentioned in the literature ,,, . These include pituitary tumours due to necrosis or apoplexy , , pineal tumours  and sphenoid meningioma  . We report a case of a previously asymptomatic and healthy female, who was operated for total abdominal hysterectomy under subarachnoid blockade and later developed possible conning due to undetected and asymptomatic preoperative intracranial tumor.
| Case report|| |
We received an intubated 55-year-old multiparous woman (gravida 3 para 4) on inotropes (dopamine 15µg.kg -1 .min -1 ) and oxygen support in our trauma and emergency department. The patient had undergone total abdominal hysterectomy and oophorectomy under subarachnoid block. On the second post operative day she had gradual deterioration in consciousness and respiration. She had to be intubated and was kept on IPPV with Bain's circuit and oxygen support. The anaesthesiologist referred the patient to our tertiary care institute for further management in view of non availability of ventilators and adequate ICU care at his centre.
As per records sent along with the patient, she had no relevant past medical history except for typical signs and symptoms of dysfunctional uterine bleed for which she was on some medications. Anaesthesia was given in the form of intrathecal bupivacaine 0.5% (heavy) 10mg with fentanyl 25mcg as adjunct using 26G Qunicke's spinal needle in L3-L4 intervertebral space under standard all aseptic conditions. At 5 min a sensory block to T6 was achieved and the operation proceeded. Systolic blood pressure ranged between 130 and 90 mm Hg and the intraoperative heart rate was stable at 65-85 beats min -1 . Boluses of mephentermine were given as required in 3 mg increments to a total of 12 mg. Intraoperatively patient maintained her vitals and was sedated (midazolam 2mg) but was arousable throughout the 90 minutes of surgery. There was no significant intraoperative blood loss. The immediate postoperative period was also uneventful except delayed return of modified Bromage score of 6 (after 8 hr). She started accepting liquids orally after ten hours of surgery without any problem.
On the second postoperative day (28 hours post operative) she complained of severe continuous headache and nausea along with photophobia. The headache did not vary with change in posture and was given some analgesic and IV fluids for it. Two hours later she became restless, agitated and aggressive. She had two episodes of projectile vomiting which contained mostly gastric material and was non blood/bile stained. This was accompanied by slurring of speech and decreased response to verbal commands. Neurological examination revealed photophobia, no meningism, no additional motor or sensory deficits and a Glasgow coma score (GCS) of 14-15/15. Systolic blood pressure at the onset of the headache was 150 mm Hg, with a heart rate of 80 beats min -1 . There was no weakness of any part of the body or any focal or generalized seizures. There was no increase in bleeding from the drains or excessive soakage.
Electrocardiogram and serum electrolytes were normal. Investigations at that time included a normal coagulation profile (prothrombin time 12.1 s, control 13.2 and activated partial thromboplastin time 30.2 s, control 32.1 1 ). and full blood count (haemoglobin 13.5 g.dl -1 , platelets 272x~10 9 litre -1 ). Anticipating an impending respiratory arrest in view of decrease in tidal volume and gasping respiration (SpO 2 <80%), she was intubated. She was kept on artificial manual ventilation and oxygen support. There was rapid deterioration in her haemodynamic status. She developed bradycardia and became hypotensive. Intravenous atropine 0.6mg and fluids (1 liter of dextrose 5% in normal saline) and injection mephentermine 12mg intravenous was followed by inotropic support (dopamine 5µg.kg -1 .min -1 and increased to 15µg.kg -1 .min -1 ). She was given intravenous augmentin 1.2 g, tramadol 50mg, dexamethasone 8mg and transferred to our hospital for further care.
Thirty two hours postoperatively when we received an intubated manually ventilated patient on inotopic support, she was hypotensive (mean arterial pressure of 50mmHg), not responding to verbal/painful stimuli with the GCS of 3-ETT/15 (E1 , VETT, and M 2 ). We immediately put her on Bird's ventilator with SIMV mode with a respiratory rate of 14/minute, FiO 2 of 0.6, pressure support of 14cm of H 2 O. Complete blood analysis, ECG, serum electrolytes and chest Xray were normal. ABG showed a pH of 7.6, pCO 2 : 21.9mmHg, pO 2 : 571.8mmHg, SO 2 %: 100%, HCO 3 : 21.7mmol/L, BE-ECF 0.0, BE-B: 2.5mmol/L. Hydrocortisone sodium 200mg was administered and mannitol infusion 1mg.kg -1 given. Fundus examination revealed undilated pupils with clear media and no signs of papllioedema. The differential diagnosis of intracranial hemorrhage, encephalitis, meningitis, metabolic derangement was made and CSF was sent for examination.
Neurologist advised CT scan which revealed a hyperdense space occupying lesion measuring 3.7 X 2.4 mm with peripheral oedema in left temporal region. It showed mild enhancement from 39HU to 58HU. A large hypodense area was also seen in the left temporoparietal region with effacement of the overlying cortical sulci. Differential diagnosis of white matter oedema or an intracerebral infarct in left temporoparietal region was kept. There was also a midline shift of 0.6cm towards right side with compression of the left ventricle and descending transtentorial herniation and diffuse cerebral oedema. Brainstem and fourth ventricle were mildly being compressed. Bilateral cerebellar hemisphere showed normal attenuation. Basal cisterns, Sylvain fissure and cortical sulci were effaced (signs of diffuse cerebral oedema).
Plan for urgent craniotomy for removal of the tumor was taken by the neurosurgical team. On discussion of the treatment plan with the patients' relatives, we could not convince them for surgery. They could not be persuaded due to financial constrains and decided to take the patient home against medical advice. She stayed in the hospital for only four hours. On follow up it was learnt that the patient expired at home the same night.
| Discussion|| |
Brain tumours (14.4%) may go unrecognized clinically  and these are the patients who may present for some surgery to be done under regional blocks. Our patient presented for total abdominal hysterectomy under spinal anaesthesia without any signs and symptoms of any intracranial lesion.
On reviewing the literature, we found only three cases of intracerebral haemorrhage ,, and one case of SAH alonev  after a subarachnoid block. The latter, described a 60-yr-old man who developed an SAH after two consecutive subarachnoid blocks within 2 weeks period. They postulated that low CSF pressure exacerbated by the second dural puncture can develop even without postdural puncture headache. The facilitation of the rupture of a potential vascular malformation might occur due to the decrease in intracranial pressure which results in an increase in transmural pressure across the arterial wall.
In our patient, severe headache occurred suddenly on the second day of a spinal anaesthetic for abdominal hysterectomy and was refractory to routine analgesics. The differential diagnosis included postdural puncture headache, caused by CSF loss and subsequent low CSF pressure. In our case, there was neither sufficient time for significant CSF loss through a 26G hole in the dura, nor any significant CSF loss during spinal needle insertion. The presentation of headache was atypical, with a sudden, severe onset and no postural element. Tension headache or migraine was unlikely because the onset of headache was too sudden and severe, with no history of similar headaches. In our patient the headache lasted several hours, extending far beyond the normal period of drug action. As the patient had rapid deterioration in the neurological and later the cardio-respiratory status, other possibilities like subarachnoid aneurysm haemorrhage, meningitis, midbrain infarction, pituitary apoplexy, encephalitis, cavernous sinus thrombosis, carotid artery aneurysm and parasellar tumors were considered. After exclusion of the common causes of headache, a computer tomogram was performed, which revealed the previously asymptomatic intracranial space occupying lesion.
Postdural puncture headache should be taken seriously and treated early and adequately to minimize the rare but potentially fatal complications. Very few reports describe intracranial haemorrhages after dural puncture and most of these are subdural haematomas ,,,, . A continuing CSF leak leads to low CSF pressure with pulling on the dura and bridging veins, causing postdural puncture headache. If this headache is left untreated, the shearing forces can lead to venous tears and which becomes treatment-resistant acute or chronic subdural haematoma. Typically, the patient presents with prolonged postdural puncture headache, with loss of the postural element, and neurological symptoms and signs develop. At this point the intracranial haemorrhage is usually diagnosed. Relatively sudden swings in blood pressure could have facilitated the rupture of a potentially weakened vessel wall before autoregulation became effective. Aneurysms are known to rupture under conditions associated with sudden rises in blood pressure  . Epidural blood patch is known to produce immediate relief in up to 89% cases of post dural puncture headaches but we were not sure if it would be of any help in our patient  . As there was already a CT scan evidence of descending transtentorial herniation and presence of diffuse cerebral oedema.
It is not ethical and routine at our institute to let an intubated patient go home, but in this case due to glaring financial constrains the patients attendants refused further treatment and insisted on leaving against medical advice. This case also highlights the socioeconomic factors which do not allow poor patients in developing countries to avail proper treatment. This case raises a lot of intriguing questions. Would a proper neurological pre anaesthesia assessment save such patients? Should proper and thorough neurological examination be advisable in every patient who has to undergo subarachnoid blockade? If an epidural catheter is considered, it should be inserted by an experienced operator to minimize the risk of a dural tap, which could be disastrous. It should be ensured that the patient be assessed thoroughly by the gynecologists and the anaesthesiologists to formulate a safe management plan.[Figure 1] and [Figure 2]
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[Figure 1], [Figure 2]