Tag Archives: neurosurgery

Algorithm: Management of Brain Metastases

Single Brain Metastases:

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Multiple Brain Metastases:

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SRS vs surgery:

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Reference:

Hatiboglu, M., Akdur, K. and Sawaya, R. (2018). Neurosurgical management of patients with brain metastasis. Neurosurgical Review.

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Algorithm for Treatment of Cerebral Venous Thrombosis (CVT)

An algorithm for the diagnosis and management of CVT:

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CTV, CT venography; CVT, cerebral venous thrombosis; ICH, intracerebral
hemorrhage; LMWH, low molecular weight heparin; MRV, magnetic resonance venography; PRES, posterior reversible encephalopathy syndrome; UHF,
unfractionated heparin.

 

Table 1 Major risk factors and conditions associated with CVT
Infection

  • INFECTION:
    • Paranasal sinusitis
    • Intracranial infections: abscess, meningitis
    • Trauma Head trauma, neurosurgical operations
    • Internal jugular catheter
  • MEDICAL / SURGICAL CONDITIONS
    • Dehydration
    • Pregnancy and puerperium
    • Coagulation disorders: factor V Leiden, protein C / S deficiency, antithrombin III deficiency, hyperhomocysteinemia, APAS
    • Hematologic disorders: polycythemia, sickle cell disease, TTP, polycythemia, PNH
    • Malignancies, inflammatory bowel disease, nephrotic syndrome, liver cirrhosis, collagen vascular disease including SLE, Wegener’s granulomatosis and Behçet syndrome
    • Previous surgical procedures
  • MEDICATION
    • Oral contraceptives, hormone replacement therapy,  L-asparagenase, corticosteroid

 

Table 3 Clinical presentations of CVT:

  • Symptoms
    • Headache
    • Double or blurred vision
    • Altered consciousness
    • Seizure
    • Behavioral symptoms (delirium, amnesia, mutism)
  • Signs
    • Papilledema
    • Focal neurologic deficit
    • Cranial nerve palsy
    • Nystagmus

 

Society of Neurointerventional Surgery (SNIS) Recommendations:

Imaging
► A combination of MRI/MRV or CT/CTV studies should be performed in patients with suspected CVT (class I; level of evidence C).
► DSA as a diagnostic modality is indicated in cases of suspected CVT when the diagnosis of CVT cannot be reliabl established with non-invasive imaging alone (class IIa; level of evidence C).

Medical and surgical treatment
► Anticoagulation with unfractionated heparin or low molecular weight heparin is reasonable in patients with CVT (class IIa; level of evidence C).
► Decompressive craniectomy may be considered in patients with large parenchymal lesions causing herniation or intractable intracranial hypertension (class IIb; level of evidence C).

Endovascular therapy
► Endovascular therapy may be considered in patients with clinical deterioration despite anticoagulation, or with severe neurological deficits or coma (class IIb; level of evidence C). The duration of anticoagulation therapy before declaring it to be a ‘failure’ and proceeding with endovascular therapy is unknown.
► There is insufficient evidence to determine which endovascular approach and device provides the optimal restoration of venous outflow in CVT. In many cases, a variety of treatment approaches is required to establish sinus patency.

 

Radiologic Findings in CVT:

  1.  noncontrast CT – hyperdensity of occluded sinuses + cerebral edema +/- ICH
  2. contrast CT – empty delta sign, HU>70% highly specific for acute CVT
  3. MRI – T2 hypointensity in acute CVT, T1 and T2 hyperintensity in subacute CVT

 

 

References

Lee, S., Mokin, M., Hetts, S., Fifi, J., Bousser, M. and Fraser, J. (2018). Current endovascular strategies for cerebral venous thrombosis: report of the SNIS Standards and Guidelines Committee. Journal of NeuroInterventional Surgery, 10(8), pp.803-810.

 

Stress Dose Steroids

WHEN IS STRESS DOSE STEROIDS INDICATED?

  • depends on history of steroid intake and likelihood of HPA supression + type and duration of surgery
  • NONSUPPRESSED HPA AXIS: 
    • < 3 weeks of steroids at any dose
    • prednisone <5mg/daily for any duration
    • prednisone <10mg every other day
    • PLAN:  continue same regimen perioperatively; no need for cosyntropin test or stress dose steroids
  • SUPPRESSED HPA AXIS
    • prednisone >20mg/day x 3 weeks or more OR Cushingoid appearance
    • PLAN:
      • give stress dose steroids based on type and duration of surgery (see below)
  • INTERMEDIATE HPA SUPPRESSION (Unknown HPA Axis suppression, previous 3 or more intraarticular or spinal steroid injections within 3 mos prior to suregery)
    • PLAN
      • evaluate HPA axis 
        • check AM cortisol (8a.m.) after 24h off steroids
        • if <5 ug/dL – likely suppressed axis; give stress dose steroids
        • if >10 ug/dL – likely no supression; continue current dose on day of surgery
        • if 5-10 ug/dL – ACTH stim test or empiric stress dose steroids
      • ACTH stim test (standard is 250 ug):
        • if serum cortisol <18 ug/dL 30 mins after ACTH – give stress dose steroids
        • if >serum cortisol >18 ug/dL 30 mins after ACTH – no stress dose steroids

 

STEROIDS BASED ON TYPE AND DURATION OF SURGERY

MINOR PROCEDURES / LOCAL ANESTHESIA – stress dose not necessary, take AM steroids

MODERATE SURGICAL STRESS: (eg. LE revascularization, total joint replacement)

  1. take AM steroids
  2. hydrocortisone 50mg IV prior to procedure, 25mg IV q8h x 24h
  3. resums usual dose after

MAJOR SURGICAL STRESS (e.g open heart surgery, proctocolectomy, esophagogastrectomy)

  1. take AM steroids
  2. hydrocortisone 100mg IV before induction of anesthesia
  3. hydrocortisone 50mg q8h x 24h
  4. taper by half per day to maintenance dose

 

 

 

Reference:

Uptodate.com. (2018). UpToDate. [online] Available at: http://www.uptodate.com/contents/the-management-of-the-surgical-patient-taking-glucocorticoids?search=stress+dose+steroids&source=search_result&selectedTitle=1~60#H6 [Accessed 25 Mar. 2018].

The PulseRider

Pulse Rider 02

 

PulseRider – stent frame opens to conform to vessel walls (see image below) designed to keep coil within aneurysmal sac, while preserving the patency of the parent vessels.  The stent is retrievable and may be repositioned.

Source: http://www.pulsarvascular.com/technology/the-pulserider/

 

Pulse Rider 01

Source: collection of author.

Mt. Fuji Sign

The Mt. Fuji sign is a radiologic finding seen in tension pneumocephalus.  Bilateral hypoattenuating collections are seen in the frontal subdural space, which causes compression and separation of the frontal lobes.

 

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Notice the widening of the interhemispheric space between the tips of the frontal lobes which resembles the silhouette of Mt. Fuji.  

 

In tension pneumocephalus, air enters into the cranial vault through disruption of the skull or skull base.  Air pressure increases within the subdural space due to a ball-valve mechanism, where air enters into subdural space but egress of air is blocked by an obstruction.

Tension pneumocephalus may occur after surgical evacuation of SDH (2.5-16%), skull base surgery, paranasal sinus surgery, posterior fossa surgery in sitting position, or head trauma.

To diagnose tension pneumocehpalus, CT findings should correlate with clinical signs of deterioration.

Peaking sign” (compression of frontal lobes without separation of frontal lobes) has also been linked to tension pneumocephalus.

Treatment includes:

  1. emergent decompression to alleviate pressure
    1. drilling burr holes
    2. craniotomy
    3. needle aspiration
    4. EVD placement
  2. administration of 100% oxygen
  3. closure of dural defects
  4. careful monitoring for clinical signs of deterioration
  5. serial CT scanning of brain

This is Mt. Fuji in Japan

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Reference

Michel, Steven J. “The Mount Fuji Sign.” Radiology 232.2 (2004): 449-450.

 

Diabetes Insipidus

Production of arginine vasopressin – by magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus.  Transported to the neurohypophysis via hypothalamo-hypophyseal tract.  Injury to these structures leads to DI.

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Triphasic response in DI:

  1. First phase – DI caused by “stunning” of the magnocellular neurons, no AVP secretion.
  2. Second phase – injured hypothalamic cells degenerate and release their stored AVP
  3. Third phase – if majority of these neurons are destroyed, permanent phase of DI begins

 

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Reference:

Schreckinger, Matthew, Nicholas Szerlip, and Sandeep Mittal. “Diabetes Insipidus Following Resection Of Pituitary Tumors”. Clinical Neurology and Neurosurgery 115.2 (2013): 121-126.

 

 

RANDOM NOTES ON Diabetes insipidus (DI)

Nephrogenic DI – renal insensitivity to vasopressin, acquired or genetic; lithium

Central DI – deficiency in production of ADH

  • Related to extent of excision
  • Usually transient phenomenon after surgery
  • SIADH in second phase – follow serum Na on day 7
  • Symptoms: polyuria, nocturia, polydipsia / thirst

 

Patients with DI, especially if drowsy and unable to maintain adequate fluid intake, can rapidly become dehydrated.


 

ALGORITHM:

Measure Is and Os hourly, sum every 6 hours

Foley catheter

Onset of dilute polyuria UOP >250cc/hr x2  hours

Check other reasons:

  1. diuretics
  2. large resuscitation
  3. mannitol
  4. hyperglycemic
  5. salt wasting

Labs

  1. USG <1.005
  2. UOsm 50-200 (<serum)
  3. Hypernatremia

? rountine serum Na – every 6 hours on day 1, then every 12h until stable, then daily x 1 week

Replace fluids

  1. normal saline to replace previous hour output, switch to 0.45% saline if UO 4-6ml/kg/h, switch to D5W if >6 ml/kg/h
  2. if awake, fluids ad libidum; may be able to maintain fluid balance by drinking to satiety, still DDAVP so patients can sleep comfortably at night

DDAVP (1-desamino-8-D-argnine vasopressin)

  • DDAVP: activates V2R – water reabsorption in kidney; mobilizes water channel aquaporin to luminal membrane of DCT and CD
  • Liquid form – given intranasal; oral tablet form; parenteral form

 

  Tablets Spray Solution for injection
Dose comparison 100 mcg 2.5 mcg N/A
200 mcg 5 mcg Less than 0.5 mcg
400 mcg 10 mcg Less than 1 mcg

 

  • Usual dose 1 ug q12h
  • Empiric – give minimum dose required to control polyuria; goal to control nocturia, partial control of polyuria during the day
  • Water retention à hyponatremia is a potential risk; patient education, serum NaHS

 

ENDOCRINE

Post-op complications: hematomas, epistaxis, HCP, CSF leaks, meningitis

Preop labs with hypopituitarism – stress doses of hormonal replacement; keep on physiological dose until outpatient assessment

Lab tests post-op for evidence of early endocrinological remission

Cushing – no steroids unless necessary; serum cortisol q6h until nadir; if <5 + symptoms, start glucocorticoid therapy and then transition to maintenance doses until outpatient reassessment

Normal cortisol function prior to surgery – no steroids; assess post-o with AM fasting cortisol on POD1 or POD2; new start steroid replacement if cortisol <10 until reassessed outpatient

Acromegaly – POD1 serum GH level predicts early remission; delayed IGF1 level 6 weeks after

Prolactinomas – POD 1 AM prolactin level normalizes with remission

 

Classification and Severity of Diabetes Insipidus

Interesting classification of DI, taken from Neurology India, groups DI into mild and severe based on some clinical and lab findings.

 

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This was their protocol for diagnosis and management of DI in patients who underwent craniopharyngioma surgery.

 

Protocol for diabetes insipidus

  • Diagnosis:  UO > 4ml/kg/h over 6 h perior OR Na >145 mEq/L with USG <1.005
  • Monitoring
    • if drowsy, unable to drink – measure Is and Os hourly, sum every 6 hours
    • Foley until UO reasonably controlled
    • intraop Na if surgery >6h determines type of IV fluids and if pitressin required in OR
    • measure Na q6h day 1
    • measure Na q12h day 2 until stable x 3 days
    • measure Na daily x 1 week
  • Treatment
    • Fluids until patient is awake and demonstrates intact thirst mechanism
      • 0.45% saline when UO 4-6 ml/Kg/h
      • D5W when UO >6ml/kg/h
    • DDAVP
      • day 1 – 5 unit IV boluses of pitressin
      • started as early as possible, usually on 2nd day, oral DDAVP 100 ug tablets of fractions of tablets
  • Adequacy of control
    • based on serum Na rather than Is and Os
      • check frequency >150 or <130 or inc/dec by >10mEg/L in 1 day

 

Other pearls:

  • Adipsia may be complication of hypothalamic damage
    • diminished thirst sensation
    • higher risk of developing hpyernatremia
    • require round the clock DDAVP
    • need to be trained to drink 2-3L water per day
    • gradually resolves with partial or complete thirst recovery by 9 months
  • Polydipsic with high UO
    • patient compensating with increased PO intake, normal or low Na
    • at risk for water intoxication or hyponatremia
    • use oral rehydration solution rather than plain water

 

Reference:

Chacko, AriG et al. “Evaluation Of A Protocol-Based Treatment Strategy For Postoperative Diabetes Insipidus In Craniopharyngioma”. Neurology India 63.5 (2015): 712.