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Year : 2008  |  Volume : 52  |  Issue : 5  |  Page : 592 Table of Contents     

Adverse Outcome in a Patient with Undiagnosed and Asymptomatic Intracranial Lesion after Total Abdominal Hysterectomy

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 Acceptance20-Jul-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
Anurag Tewari
126-D, Kitchlu Nagar, Ludhiana, Punjab,141001
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Source of Support: None, Conflict of Interest: None

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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 Top

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 [1],[2] . Diagnosis of a brain tumour after spinal anaesthesia is rare [3] ; how­ever, a few cases have been mentioned in the litera­ture [4],[5],[6],[7] . These include pituitary tumours due to necrosis or apoplexy [4],[6] , pineal tumours [5] and sphenoid menin­gioma [7] . 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 Top

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 Top

Brain tumours (14.4%) may go unrecognized clini­cally [8] 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 [9],[10],[11] and one case of SAH alonev [12] 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 [13],[14],[15],[16],[17] . 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 [18] . 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 [19] . 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]

   References Top

1.Auroy Y, Benhamou D. Major complications of regional anaesthesia in France. Anesthesiology 2002; 97: 1274-­80.  Back to cited text no. 1      
2.Auroy Y, Narchi P, Messiah A, et al. Serious complica­tions related to regional anaesthesia results of prospective survey in France. Anaesthesiology 1997;87: 479-­86.  Back to cited text no. 2      
3.Ercan Ozer, et al. Initial presentation of prostatic adeno­carcinoma after spinal anaesthesia as a falcian mass, Journal of Neurlogical Sciences (Turkish) 2004 ;21:27­-32.  Back to cited text no. 3      
4.Bria A, Berger A, Pepcak F. Pituitary necrosis after spi­nal anaesthesia: A case report. Ann Endocrinol Paris 2000 ;61 : 164-7.  Back to cited text no. 4      
5.Dutton DA. A post spinal headache associated inci­dental intracranial pathology, a case report. Anaesthesia 1992; 47: 450-1.  Back to cited text no. 5      
6.M Lennn, P Seigne, AJ Cunningham. Pitutary apoplexy after spinal anaesthesia. British Journal of Anaesthesia 1998;81: 4616-618.  Back to cited text no. 6      
7.Marghade PL, Gvalani S, Jedge P, Pandya SH, Dewoolkar LV. Incidental diagnosis of sphenoid meningioma after spinal anaesthesia. The Internet Journal of Anesthesiology 2007;12:2.  Back to cited text no. 7      
8.Mierzejewska E. Clinical pattern of malignant brain tu­mors in patients over 50 years of age. Neurol Neurochir Pol 1976; 10:738-42.  Back to cited text no. 8  [PUBMED]    
9.Benzon HT. Intracerebral hemorrhage after dural punc­ture and epidural blood patch: nonpostural and non­continuous headache. Anesthesiology 1984; 60: 258-9.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Antia AM. Clinical report of the occurrence of an intrac­erebral hemorrhage following post-lumbar puncture headache. Anesthesiology 1981; 55: 684-5.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]  
11.Wedel DJ, Mulroy MF. Hemiparesis following dural puncture. Anesthesiology 1983; 59: 475-7.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Bottiger BW, Diezel G. Akute intrakranielle Subarachnoidalblutung nach wiederholter Spinalanasthesie. Anaesthesist 1992; 41: 152-7.  Back to cited text no. 12      
13.Pavlin DJ, McDonald JS, Child B, Rusch V. Acute sub­dural hematoma-an unusual sequelae to lumbar punc­ture. Anesthesiology 1979; 51: 338-40.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]  
14.Newrick P, Read D. Subdural haematoma as a complica­tion of spinal anaesthetic. Br Med J 1982; 285: 341-2.  Back to cited text no. 14      
15.Edelman JD, Wingard DW. Subdural hematomas after lumbar dural puncture. Anesthesiology 1980; 52: 166- 67.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]  
16.Skoldefors EK, Olofsson CI. Intracranial subdural haematoma complicates accidental dural trap during labour. Eur J Obstet Gynecol Reprod Biol 1998; 81: 119- 21.  Back to cited text no. 16      
17.Vaughan DJA, Stirrup CA, Robinson PN. Cranial sub­dural haematoma associated with dural puncture in labour. Br J Anaesth 2000; 84: 518-20.  Back to cited text no. 17      
18.Pulsinelli WA. Cerebrovascular diseases, aneurysmal subarachnoid hemorrhage. In: Bennett JC, Plum F, edi­tors. Cecil's Textbook of Medicine. Philadelphia: W. B. Saunders, 1996; 2073-6.  Back to cited text no. 18      
19.DiGiovanni A, Dunbar B. Epidural injections of autolo­gous blood for post dural puncture headache. Anesth Analg 1970; 49: 226-32.  Back to cited text no. 19      


  [Figure 1], [Figure 2]


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