Surgery

Question 1

HIRSCHSPRUNG’S DISEASE

Answer 1

CLINICAL PRESENTATION
More than 85% of cases present in the neonatal period usually with delayed passage of meconium bevond the first 24 hours of life, abdominal distention, and bilious vomiting. I
is often complicated by enterocolitis, which may result in perforation and septicemia.
Older children (Us0aty distention assoct od
ars)
: with chronic constipation and abdominal aemia
. PRE: anal spasm, empty rectum, and in case of enterocolitis there is explosive discharge of foul smelling fluid stool and gas.
INVESTIGATIONS
. Erect abdominal X-ray: Distended bowel loops with Paucity of air in the rectum.
Contrast enema: reveals narrow distal segment (aganglionic) and dilated proximal colon (ganglionic) with a funnel - shaped transitional zone in between.
• Anorectal electromanomertry: There is no relaxation of the internal anal sphincter i response to rectal distention by a balloon.

. Rectal biopsy
The confirmation of the diagnosis is based on the histological examination of rectal wall biopsy specimen which reveals absence of ganglion cells in myentric (auerbach) and
submucosal (meissner) plexus with presence of an excess of hypertrophied cholinergic nerves.
TREATMENT
The treatment is surgical but preoperative stabilization isimportant.
Resuscitation: patients presented with intestinal obstruction should be resuscitated with nasogastric tube, intravenous fluld, antibiotics, and repeated emptying of the rectum with
rectal tube and irrigation.
Colostomy: end colostomy proximal to the transitional zone with frozen section blopsies
Definitive pull-through procedures
The p the arocedure is resection of the aganglionic segment of the
colon followed by sneliogic colon down to the anal canal. puiting tne şalnS
Swenson procedure (rectosigmoidectomy) Duhamel procedure ( retrorectal pullthrough)
Soave procedure (endorectal pullthrough)
Transanal endorectal pullthrough as one stage operation without colostomy but not in
delayed cases or in emergency cases.
LATE COMPLICATION

Enterocolitis
volding dysfunction
Chronic constipation
Fecal incontinence

Question 2

MECKEL’S DIVERTICULUM

Answer 2

MECKEL’S DIVERTICULUM
The most common congenital malformation ofthe small intestine.
It is a true diverticulum contain all layer of small bowel on the antimesenteric border.
INCIDENCE
2% of population. M: F ratio 2:1
About 2 years old.commonly
PATHOPHOPHYSIOLOGY
• 2 feet from ileocecal valve.
2 cm in diameter, 2 inches in length.
• Contain 2 hetrotopic tissue (gastric and pancreatic)
CLINICAL PRESENTAON 1.Asymptomatic(incidentally)
2.Haemorrhage:
•. Commonest presentation.65%.
• Preschool child with painless maroon color rectal bleeding, episodic, ceases usually
spontaneously.
• Sometime only iron deficiency anemia.
3.0bstruction: - secondary to Intussusception or volvulus. 4.Diverticulitis(inflimation):

Features mimic acute appendicitis but less intensity of nausea &vomiting and maximum tenderness may migrate across the abdomen when the child moves and
previous same pain. 5.Less common:
• Littre’s hernia, intra-abdominal hemorrhage or cystic mass.
DIAGNOSIS
|- History & cxanmination.
2- NGT to cxclude upper GI blccding.
3- PR & occasionally lower cndoscopies to cxclude lower GI bleeding.
4- Radiology for complications e.g. obstruction or intestinal inflammation caused by diverticulitis. Enenma, U/S & CT scan for Intussusception.
5- Meckel’s scan (Technetium 99m pertechnetate). 6- Laparoscopy or laparotomy.
7- Angiograph >invasive, ulcer should be actively bleeding. 8- Wircless capsule endoscopy.
TREATMENT
1. Laparoscopic diverticulectomy.
• Narrow base > diverticulectomy.
• Wide base > resection & intra or extracorporeal anastomosis.
2.
.incidental meckels:
Male. larger than 2 cm,contain gastric tissue, younger age
Appendicectomy.

Question 3

intussusception

Answer 3

PRESENTATIONS
• The classic presentation of intussusception is a young child with intermittent, crampy abdominal pain associated with “currant jelly” stools and a palpable mass on physical examination, although this triad is seen in less than a fourth of children.
• Abdominal pain: acute, cramping; stiffen & pull legs to the abdomen > free of pain and the attack usually occure every 15-30 minute ,the child between the attack healthy and later on become lethargic on recurrent attacks and the attack ceases as it started .
• Vomiting: almost universal, later on become bilious.
• Bowel motion: small & normal initially > stool tinged with blood > dark-red mucoid clots
(currant-jelly stool).
I

EXAMINATION
• Flat or empty RLQ (Dance`s sign).
• During relaxation, sausage shape or curved mass can be felt anywhere in the abdomen,
especially in the right upper quadrant or epigastrium.
• PR > blood stained mucus or fresh blood & palpable mass.
• Delayed > signs of dehydration and bacteraemia with tachycardia and fever and signs of
peritonitis.
• Grave sign > intussusceptions through anus may mimic rectal prolapse: .
Blade can be passed more than 1-2 cm through the anus suggesting intussusception.
DIAGNOSTIC STUDIES
1- PlainAXR:-
• Abnormal distribution of gas & fecal content.
• Sparse large bowel gas and absence of caecal gas.
• Air fluid level.
• Mass.
2- U/S:-highsensitivityandspecificity.
• Target lesion on transverse section: 2 rings of low echogenicity separated by hyper
echoic ring.
• Pseudo-kidney sign on longitudinal section.
• Lymph node enlargement.
• Free intra peritoneal fluid.
.
3- Bariumenema:
• Claw sign.
• Coiled spring sign.
4- Colored Doppler:
• To assess the vascularity of intussusception. 5- CTscanorMRI.
II

NON-OPERATIVE MANAGEMENT:
1. Nothing per oral.
2. NG tube.
3. I.V fluid.
4. Antibiotics.
5. F.B.C & s.electrolytes.
6. Reduction.
Hydrostatic reduction.
By using barium enemaunder fluoroscopic monitor but due to risk of perforation and barium peritonitis(85% fatality rate) for that reasoned recently use water soluble contrast under fluoroscopic guide with successful rate 85% in uncomplicated case.
Pneumatic reduction.
By using air 80-120mmHg ,the pneumatic reduction is used under fluoroscopic monitor and successful in 90% of uncomplicated cases.
It is faster than hydrostatic and safer and decrease the time of radiation exposure
The disadvantage was perforation>pneumo peritoneum.
OPERATIVE MANAGEMENT: • Indications:
1. Evidence of peritonism or perforation, sepsis or possible gangrenous bowel.
2. Evidence of lead points e.g. filling defect on contrast enema.
3. Delayed presentation with persistent hypotension
4. Failure of non-operative management.
5. Perforation during non-operative reduction.
RECURRENT INTUSSUSCEPTION:
• The majority within 6 months.
• Usually have no lead points.
• Less with surgical reduction.
POSTOPERATIVE INTUSSUSCEPTION:
• Intussusception occurs after operations done for a variety of conditions e.g., thoracic or abdominal.
• May not been diagnosed preoperatively (adhesion).
• Usually within a month.
• Most > ileoileal.

Question 4

IMPERFORATE ANUS

Answer 4

IMPERFORATE ANUS
Imperforate anus is the absence of a normal anal opening. The diagnosis is usually made shortly after birth by a routine physical examination. Imperforate anus occurs in about 1 in 5000 births.
CLASSIFICATION ( of anorectal malformations )
• Recto-urethral fistula (male)
• Rectovesical fistula (male)
• Recto-vestibular fistula (female)
• Persistent cloaca (female)
• Recto-perineal fistula.
• Imperforate anus without fistula.
• Rectal atresia.
The most frequent defect in male patients is recto-urethral fistula; while in female is Recto- vestibular fistula.
ASSOCIATED anomaliese (40%)
• Sacral and spinal cord anomalies.
• Genitourinary malformations.
• Congenital heart disease.
• Esophageal atresia and tracheo-esophageal fistula.
• Down syndrome
INITIAL MANAGEMENT
Resuscitation
• Nil by mouth, naso-gastric tube
• Intravenous fluid, antibiotics
• incubator
Measures to exclude associated anomalies
• X-ray of the spine, and U/S spine.
• U/S abdomen.
• Echocardiogram.
• Naso-gastric tube placement to exclude tracheo-esophageal fistula.

Perineal inspection
Meconium on the perineum indicates perineal fistula while meconium in the urine indicates recto-urinary fistula.
Radiological evaluation:
•
• •
Cross-table lateral plain x-ray with the baby in prone position to see the distance between the rectal gas and the perineal skin.
invertogram
Should be done 24 hours after childbirth because before that the rectum is collapsed and need significant intra-luminal pressure to overcome the tone of the muscle surrounding the lower part of the rectum.
SURGICAL TREATMENT
➢ In case of recto-perineal fistula or the distance between the rectal gas and the perineal skin is less than 1 cm; the surgical treatment is anoplasty and no need for colostomy.
➢ In all othercases; the surgical treatment consist of three stages:
1. Colostomy: double barrel ,lower descending or upper sigmoid colostomy 2. Posterior sagittal anorectoplasty
➢ Pulling the rectum anterior to the puborectalis muscle, then the rectum is sutured to the skin of the perineum in its normal position.
➢ Two weeks after the repair, anal dilatations are started with special dilatation program to prevent stricture
3. Colostomy closure: when anal dilatations reach the desired size according to the patients age.
LATE COMPLICATIONS
• Incontinence
• Constipation
• Voiding dysfunction

Question 5

PYLORIC STENOSIS

Answer 5

CLINICAL FEATURES
❖
❖
❖ ❖ ❖
❖ ❖ ❖
❖ ❖
The classic presentation is nonbilious, projectile vomiting in a full-term neonate who is between 2 and 8 weeks old. Initially, the emesis is infrequent and may appear to be reflux. However, over a short period of time, the emesis occurs with every feeding and becomes forceful (i.e., projectile). The contents of the emesis are usually the recent feedings, but signs of gastritis are not uncommon (“coffee-ground” emesis). The vomiting is typically non-bilious and the infant is typically hungry after vomiting, eager to eat, only to vomit once again.
The presentation is slight later in preterm infants and only 4 % present at an age older than 3 months. Failure to thrive.
Constipation.
The degree of dehydration depend on the rapidity of diagnosis.
Visible peristaltic waves may be present in the mid to left upper abdomen.
Scaphoid abdomen.
Palpable right upper quadrant olive is very important sign75-90%.
Feeding teset: when the infant completely relax (some time do flexion of the hip)and using pacifier with sugar water palpate the olive mass of the pyloric in the epigastric or Rt hypochondrial.
DIFFERENTIAl DIAGNOSIS
1. Pylorospasm.
2. Gastroesophageal reflux.
3. Gastroenteritis.
4. Increased intracranial pressure.
5. Metabolic disorders.
6. Anatomic causes e.g. an antral web, foregut duplication cyst.
IMAGING
A. U/S:
• Sensitivity 97 %, specificity 100 %.
• The diagnostic criteria for pyloric stenosis is a muscle thickness of greater than or equal to 4 mm and
a length of greater than or equal to 16 mm.
• Distinguish pylorospasm (periods of relaxation).
I

B.
• • •
upper GI series (an equivocal ultrasound study): String sign.
Double track sign(shouldering sign).
Delayed gastric emptying.
PREOPERATIVE PREPARATION
❖ ❖
❖
❖
❖ ❖
❖
The mainstay of therapy is typically resuscitation followed by pyloromyotomy.
There are reports of medical treatment with atropine and pyloric dilation, but these treatments require long periods of time and are often not effective.
Initially, a 10-20-mL/kg bolus of normal saline should be given if the electrolyte values are abnormal. Then D5/1⁄2NS with 20 to 30 mEq/L of potassium chloride is started at a rate of 1.25 to 2 times the maintenance rate.
Electrolytes should be checked every 6 hours until they normalize and the alkalosis has resolved. Then the patient can safely undergo anesthesia and operation.
It is important to appreciate that HPS is not a surgical emergency and resuscitation is of the utmost priority.
NGT is controversial, but may be used for severely distended stomach and to prevent aspiration following contrast study and in case of perforation postoperatively.
Preoperative antibiotic is controversial, not with standard incision.
OPERATIVE MANAGENENT (Ramstedt`s, 1912)
❖ Evacuation of the stomach in the OR.
❖ Either open or laparoscopic pyloromyotomy.
❖ Avoid opening mucosa.
POSTOPERATIVE MANAGEMENT
❖ NGT is not necessary unless the mucosa has been entered.
❖ Feeding begins 4-6 hours after operation with G/W low volume, gradually increasing to full feeds over
the next 12-24 hr. if vomiting, same volume can be repeated.
❖ Discharged the day after operation.
POSTOPERATIVE COMPLICATIONS
❖ Unrecognized mucosal perforation.
❖ Wound infection and dehiscence.
❖ Postoperative emesis is common, occurring in up to 80% of patients at some point. Prolonged emesis is
less common is usually due to Gastroesophageal reflux or secondary to incomplete myotomy or due to gastric atony.

Question 6

Paediatric Neurosurgery

Cyst types

Answer 6

Cyst types
• Arachnoid cyst – typically middle fossa, CSF enclosed in an
envelope of arachnoid mater.
• Colloid cyst – occurs in the roof of the third ventricle, believed to
represent embryonic endoderm remnants.
• Dermoid and epidermoid cysts – epithelial lined structures arising
from displaced ectodermal remnants, typically in the posterior fossa
(midline) and cerebellopontine angle, respectively.
• Porencephalic cysts – brain cavities lined with gliotic white matter,
containing CSF in communication with the ventricles or subarachnoid
space.

Question 7

Paediatric Neurosurgery

Posterior fossa malformations

Answer 7

Posterior fossa malformations
Chiari malformations involve cerebellar herniation through the
foramen magnum:
• Normal: Up to 5 mm of cerebellar tonsillar descent through the
foramen magnum
• Chiari I: >5 mm of tonsillar descent: presents typically in
young adults with headache and variable neurological
disturbance
• Chiari II: descent of the tonsils and vermis: presents in infancy
with poor feeding, stridor and apnoeic episodes.
They are often associated with syringomyelia, the presence of a fluid-filled
cavity (syrinx) in the spinal cord. Compression of the brainstem and
cerebellum, or development of a syrinx, may cause neurological deficits.
Shunting and foramen magnum decompression are the mainstay of
treatment. Chiari malformations may also present incidentally or with
headaches exacerbated by valsalva.
Dandy Walker malformations present in infancy with macrocephaly,
developmental delay and hydrocephalus; most patients have associated
abnormalities in the CNS and other organ systems. Imaging demonstrates a
hypoplastic cerebellar vermis, with the posterior fossa occupied by a large
thin-walled cyst. Treatment usually involves shunt placement.

Question 8

Paediatric Neurosurgery

Craniosynostosis

Answer 8

Craniosynostosis
Normal fusion of the coronal, lamdoidal, squamosal and sagittal
sutures occurs between six and 12 months of age; others, such as
the frontal suture fuse later . Craniosynostosis is the premature fusion
of one (simple craniosynostosis) or more (complex craniosynostosis)
cranial sutures, preventing growth perpendicular to the suture. This
results in a range of skull deformities and hydrocephalus. Syndromic
craniosynostosis, often associated with abnormalities of the
fibroblast growth factor receptor genes, is accompanied by
developmental delay and other abnormalities. The surgical treatment
aims to correct deformity and prevent development of raised ICP

Question 9

Paediatric Neurosurgery

Neural tube defects

Answer 9

Neural tube defects
Failure of closure of the neural tube is associated with folate deficiency, family history and
some anticonvulsants.
**Prenatal screening, using serum alphaprotein levels and ultrasound, and diagnostic
testing, using amniocentesis, are possible.
**The spectrum of conditions associated with failed closure of the posterior neuropore
includes:
• Spina bifida occulta: a congenital absence of a spinous process, without exposure of
meninges or neural tissue, but presenting a characteristic shallow hair-covered hollow at
the base of the spine. This is common and rarely clinically significant. Sometimes it may be
associated with tethered cord syndrome,which involves thickening of the filum terminale,
resulting in traction on the cord. Presentation is with progressive deficits, spasticity,
bladder dysfunction or scoliosis, and treatment involves surgical exploration and
untethering of the cord.
•. Meningocoele: a sac of meninges, covered by skin and containing
CSF alone, herniates through an anterior or posterior bony defect.
• Myelomeningocoele: a herniating sac of meninges without
covering skin contains spinal cord, nerves or both. This is always
associated with Chiari II malformation. Open myelomeningocoele
presents a high infection risk and requires early surgical repair.
• Lipomyelomeningocoele: adipose tissue adherent to the spinal
cord herniates through a bony defect to the sacrolumbar soft tissue.
This may be associated with bladder dysfunction and requires
surgical relief of the resultant cord tethering.
Failure of closure of the anterior neuropore
produces anencephaly, which is uniformly fatal –
the spectrum of spinal dysraphisms, however, is
replicated in the skull. Cranium bifidum is a failure
of fusion, often in the occipital region. This may be
associated with herniation of meninges and CSF
(meningocoele), and potentially also brain
substance (encephalocoele)

Question 10

Meningitis and ventriculitis

Answer 10

Meningitis and ventriculitis
Meningitis describes inflammation of the meninges of the brain and
spinal cord, most commonly and most seriously due to bacterial
infection.
**Community-acquired bacterial meningitis typically presents with
fever, meningism (headache, neck stiffness and photopho- bia) and
deterioration in conscious level. **The natural history involves a rapid
progression to subpial encephalopathy, venous thrombosis, cerebral
oedema and death. Therefore empirical intravenous antibiotic therapy
should be commenced as soon as the diagnosis is suspected.
**Urgent lumbar puncture is required to confirm the diagnosis and
ultimately to guide treatment. Since the differential diagnosis of this
presentation includes abscess, empyema and subarachnoid
haemorrhage, initial CT imaging, where available immediately, is
desirable to confirm that lumbar puncture is necessary and safe.
Meningitis and ventriculitis
improved mortality and neurological outcome associated
with administration of steroids (dexamethasone 0.15 mg/
kg up to 10 mg four times daily for 4 days).
**The common organisms responsible for spontaneous
bacterial meningitis are Streptococcus pneumonia,
Haemophilus influenzae and Neisseria meningitides,
Neonates are susceptible to group B streptococcus,
Escherichia coli and Listeria.
Meningitis
**Meningitis in the context of surgery typically follows a more insidious
course, but remains a feared complication requiring prompt
intervention. Typical organisms are Staphylococcus aureus,
Enterobacteriaceae, Pseudomonas and Pneumococci.
**Meningitis after head injury is common, affecting 25 per cent of
patients with base of skull fracture and CSF leak. Repair of the CSF leak
may be required, and empirical antibiotics should have activity against
commensal nasal organisms including Gram-positive cocci and Gram-
negative bacilli in the presence of symptoms/signs of clinical meningitis.
Ventriculitis refers to infection in the ventricles, commonly as a complication of meningitis or due to
contamination from a shunt or external drain. Where a drain is present, treatment may include
administration of intrathecal antibiotics through it
Meningitis summary
■ A feared complication of neurosurgery and of head injury
■ Clinical diagnosis is supported by CT to exclude other
pathology
■ CSF samples are taken for glucose and protein assay, and
for microscopy and culture
■ Treatment, pending identification of an organism, is with
broad-spectrum antibiotics

Question 11

Brain abscess and empyema

Answer 11

Brain abscess and empyema
Abscesses arise when the brain is exposed directly,
for example as a result of fracture or infection of an air
sinus, or at surgery. They also result from
haematogenous spread, typically in association with
respiratory and dental infections, or endocarditis. In 25
per cent of cases, no underlying primary infection is
found. The organisms involved are normally bacteria.
Imunnoconpromised hosts in particular are vulnerable to a broad range of
pathogens:
• sinus/mastoid infection: aerobic and anaerobic Streptococci; Bacteroides;
Enterobacteria; Staphylococci; Pseudomonas;
• haematogenous spread: Bacteroides; Streptococci;
• penetrating trauma: Staphylococcus aureus; Clostridium;
Bacillus; Enterobacteria;
• food contamination: toxoplasma, pork tapeworm (producing
neurocysticercosis);
• immunocompromise e.g. HIV/AIDS: protozoal (e.g
toxoplasma), fungal (e.g Cryptococcus), viral (e.g. JC virus producing multifocal
leukoencephalopathy) and mycobacterial abscesses are encountered.
Early cerebritis (day 3–5) is
characterised by neutrophil infil- tration
. This progresses to a late
cerebritis with necrosis, oedema and
macrophage recruitment (day 5–14)
. After this the abscess is
walled off by a develop- ing
collagenous capsule which matures
over weeks and months.
Diagnosis of brain abscess
**Patients present with the triad of features associated with mass lesions; these
are focal deficits, seizures and raised ICP.
**A typical history might include fever and malaise, progressing over hours or
days to drowsiness and confusion, then focal weakness or seizure.
**Low-grade pyrexia and equivocal blood markers of inflammation are typical;
**blood cultures should be obtained at an early stage.
**CT scan with contrast is the initial imaging modality of choice, and this will
demonstrate a well-defined ring-enhancing mass (i.e. the edge enhances on the
post-contrast images), typically with a thin smooth wall. The distinction between
abscess and tumour can be difficult and has important management implications,
since abscesses generally require urgent drainage.
**Diffusion-weighted MRI is a valuable tool in this context
Management of brain abscess
The mainstay of management of bacterial abscesses is early surgical
drainage, involving needle aspiration through a burrhole with or without
image-guidance, or by craniotomy. Intravenous antibiotic therapy is
then commenced, using broad-spectrum agents initially then tailoring
to the sensitivity of organisms cultured. Treatment should last at least 6
weeks, but a switch to oral therapy may be appropriate after an interval
and in consultation with microbiology. Mortality with prompt treatment
is about 4 per cent, but if the abscess is allowed to rupture into a
ventricle mortality it is over 80 per cent. Up to 50 per cent of patients
with brain abscess will develop seizures at some stage, so that
prophylactic anticonvulsants should be considered
Brain abscesses
■ Presenting features are those
of infection and of intracranial
mass lesion
■ Imaging reveals a ‘ring-
enhancing lesion’, with tumour
usually the main differential
■ Early diagnosis, usually
followed by drainage, is key for
good outcome
The right frontal lesion
evident on T2 magnetic reso-
nance imaging (MRI) (main
image) exhibits high signal
on DWI MRI sequences (top
right inset) indicative of
r e s t r i c t e d d i f f u s i o n
suggestive brain abscess.

Question 12

Subdural empyema

Answer 12

Subdural empyema refers to an infective collection in the subdural space and
and may develop as a result of sinusitis, mastoiditis or meningitis, and can
complicate trauma or surgery. A subdural empyema associated with
osteomyelitis of the frontal bone and associated scalp swelling, and called a
‘Pott’s puffy tumour’. In empyema, pus will generally collect in the parafalcine
region and over the convexity, triggering inflammation and thrombosis in the
cortical veins which helps to explain the high mortality of 8–12 per cent.
Presentation mimics that of meningitis and cerebral abscess; typical CT
appearances are of hypodense or isodense subdural collection, with contrast
enhancement at the margins, and a degree swelling and midline shift. The
empyema may be difficult to visualise, especially on non-contrast CT.
***Given the risk of herniation, LP should not be performed.
Subdural Empyema Craniotomy or craniectomy allows drainage of the
collection and relieves raised ICP and is the treatment of choice. Burrhole
drainage, and occasionally intravenous antibiotics without surgi- cal
intervention, may also be considered
Subdural empyema summary
■ Presenting features are similar to those of meningitis or cerebral
abscess
■ Typically a crescentic collection with a contrast-enhancing rim is
evident on CT
■ Drainage is the mainstay of treatment
Axial computed tomography
scan with contrast showing
a r i g h t h e m i s p h e r e
subdural empyema (short
arrow) and a right frontal
Pott’s puffy tumour (long
arrow) (osteomyelitis of the
frontal bone).

Question 13

Intracranial infection
TB

Answer 13

Tuberculosis
Tuberculosis (TB) infection of the central nervous system (CNS) is
believed to represent haematogenous spread from primary pulmonary
foci. A high index of suspicion is required, especially when population
or individual risk factors are present. TB can result in a diverse but
overlapping spectrum of pathology, including in the head:
• Tuberculous meningitis this commonly affect young children; CT
demonstrates intense meningeal enhancement, and hydrocephalus is
a common sequel.
• Tuberculoma – discrete tumour-like granulomas at the base of the
cerebral hemispheres, presenting with mass effect
Tuberculosis
• Tuberculous abscess – seen predominantly in
immunocom- promised hosts, this represents
progression of a tuberculoma with prominent central
caseating necrosis.
• Miliary tuberculosis – describes a diffuse distribution
of multiple small tuberculomas through brain substance.
Tuberculosis
**Where the meninges are involved, lymphocytes can be expected to
predominate in the CSF, rather than the polymorphs seen with other
bacterial meningitides.
**The increase in protein content and reduction in glucose concentration
are also less marked.
***Ziehl–Neelsen staining for myobacteria is frequently negative, and
polymerase chain reaction (PCR) testing offers relatively rapid diagnosis
compared to culture for acid-fast bacilli which may take weeks.
Management is with anti-tuberculous therapy; hydrocephalus may require
shunt insertion.

Question 14

Glioma

Answer 14

Glioma
These are tumours of glial cell origin, with subtypes
including astrocytomas, oligodendrogliomas,
ependymomas and mixed tumours.
**The diagnosis is histological, but imaging often predicts
both a glial origin and the grade of tumour) MRI with and
without contrast is the preferred modality. If the diagnosis
is in doubt, a whole-body CT scan and liver function tests
may be required to help exclude an extracranial primary.
**Initial management should generally include steroids to
alleviate any mass effect, and antiepileptics where seizures
are a presenting feature, or are likely in view of temporal
location.
**Definitive treatment depends on the likely tumour grade
in view of presentation and imaging findings. Gliomas,
except for the grade I pilocytic astrocytoma which typically
occurs in children, are notable for their diffuse infiltration
into surrounding brain, so that recurrence after even
macroscopically complete resection is the rule.
Low grade glioma (WHO Grade II) has a peak incidence in the fourth
decade of life. Historically a ‘watch-and-wait’ strategy, with or without
initial biopsy to confirm the diagnosis, has been applied. This reflects the
natural history of progression to high grade tumour over a variable
period, usually several years. The alternative, now more generally
favoured, approach is to pursue initial complete macroscopic resection
where feasible. However, this is based on limited evidence that
progression is delayed and survival prolonged by this approach. Where
tumours encroach on eloquent cortex, especially the speech areas of the
dominant hemisphere, awake craniotomy allows mapping of function
with surface electrodes at operation, to limit resection and minimise
postoperative deficit
**High grade gliomas include anaplastic astrocytomas (WHO grade III)
and glioblastomas (WHO grade IV), the most common glial tumour
**They present de novo with peak incidence in the fifth and sixth
decades of life respectively, or may represent transformation of
previously diagnosed, or clinically silent, low grade gliomas.
**Active treatment consists of maximal resection, high- dose-focused
radiation therapy, and chemotherapy administered locally as carmustine
wafers at the time of resection, or systemi- cally with oral temozolomide.
Median survival for glioblastoma remains just over 12 months.
***Solitary metastasis represents a differential diagnosis for many
gliomas, so that a chest x-ray is an important component of the work-up,
and if the diagnosis is in significant doubt a whole-body CT and liver
function tests to exclude an extracranial primary are required.
Tissue of origin for brain metastases (approximate)
Origin Percentage
Lung 40
Breast 15
Melanoma 10
Renal/GU 10
Other Unknown 25

Question 15

Meningioma

Answer 15

Meningioma
Meningiomas are usually benign lesions, although anaplastic variants
do occur. They arise from the meninges, and typically present due to
mass effect from the tumour, compounded by vasogenic oedema in the
adjacent brain and obstructive hydrocephalus where CSF drainage is
impaired. Imaging will demonstrate a contrast-enhancing mass distinct
from the brain with a dural base .
These are generally slow-growing lesions: smaller lesions,perhaps
detected incidentally in an elderly patient, may well warrant a ‘watch-
and-wait’ approach. If the lesion is large or positioned so as to impinge
on key structures, the patient may require steroids and early surgery.
Meningioma
**The degree of resection predicts recurrence,
with rates of 10 per cent at ten years for total
excision with a clear dural margin and 30 per cent
at ten years for subtotal excision.
**Lesions which are difficult to approach
surgically may be managed with radiotherapy or
stereotactic radiosurgery
Common brain tumours summary
■ Metastases and gliomas are common tumours arising within brain substance,
appearing as ‘ring-enhancing’ lesions on contrast CT. Surgery is usually life-
extending rather than curative
■ Meningiomas arise from the meninges around the brain and typically enhance
uniformly on contrast CT. Most are benign and amenable to curative resection
■ MRI brain is optimal for evaluation of these lesions. Diffusion-weighted
sequences help to exclude abscess when glioma or metastasis is suspected
■ Where metastasis is suspected, CT of the body may demonstrate the primary
lesion and allow staging
■ Steroids are administered to control swelling and mass effect in the short term

Question 16

Pituitary tumours

Answer 16

Pituitary tumours
Most tumours in this region are benign pituitary adenomas, although
the differential includes malignant variants, craniopharyngioma,
meningioma, aneurysm and Rathke’s cleft cyst .
**Microadenomas are less than 10 mm in size and usually present
incidentally or with endocrine effects.
**Macroadenomas are larger than 10 mm, and often present with
visual field deficits. Thirty per cent of adenomas are prolactinomas,
20 per cent are non-functioning, 15 per cent secrete growth
hormone and 10 per cent secrete adrenocorticotropic hormone
(ACTH)
Pituitary tumour
**Features of note in the initial assessment include any history of
galactorrhoea (suggestive of prolactinoma), and Cushingoid or
acromegalic features pointing to ACTH- or growth hormone- secreting
tumours, respectively.
**Baseline assessment of pituitary function should include serum
prolactin, follicle-stimulating hormone and luteinising hormone together
with testosterone in males or oestradiol in females, thyroid function tests,
and fasting serum growth hormone and cortisol.
**Preoperative prolactin levels are crucial since prolactinomas may be
managed without the need for surgery. The cortisol level is also important,
since deficiency must be corrected especially in the perioperative period.
Pituitary tumour
**Diagnosis of ACTH-secreting tumours can be difficult,and may
require the use of specialised tests, such as petrosal sinus sampling
and the dexamethasone suppression test.
Effective treatment requires close cooperation between the
neurosurgical team and an endocrinologist.
**Prolactinomas are managed initially with dopamine agonists,
such as bromocryptine and cabergoline.
**Growth hormone- secreting tumours may also respond to
dopamine agonists, or to somatostatin analogues, such as
octreotide.
Pituitary tumour
**Surgical resection is usually performed by a transsphenoidal approach,
using a microscope or endoscope. Sometimes large tumours also require a
craniotomy.
**After operation, patients are at risk of CSF leak (3 per cent) and pituitary
insufficiency.
***Diabetes insipidus resulting from manipulation of the pituitary stalk is
common in the immediate postoperative period and usually resolves
spontaneously. Where it is suspected, the patient will require hourly
measurement of urine output, and blood and urine samples for calculation of
sodium concentration and osmolality. If confirmed, the condition can be
managed with desmopressin in consultation with endocrinology.
Urgent intervention is generally reserved for patients with deteriorating vision.
Pituitary tumour
Pituitary apoplexy is the syndrome associated with
haemorrhagic infarction of a pituitary tumour. It
presents with sudden headache, visual loss and
ophthalmoplegia with or without impaired
conscious level. Intravenous steroids and urgent
surgical decompression are required.

Question 17

Vestibular schwannoma (acoustic neuroma)

Answer 17

Vestibular schwannoma (acoustic neuroma)
These are nerve sheath tumours arising in the
cerebellopontine angle, which present with hearing loss,
tinnitus and balance problems.
**Facial numbness and weakness are less common,
while large tumours may present with features of
brainstem compression or hydrocephalus.
**The differential diagnosis includes meningioma,
metastasis and epidermoid cyst
Vestibular schwannoma (acoustic neuroma)
**Small intracanalicular tumours (within the internal auditory canal) may be
managed with surveillance.
**For intermediate size tumours, radiosurgery is an alternative to operation.
**Large lesions (>4 cm), especially with brainstem compression, will
require excision and consideration of ventriculoperitoneal shunt to relieve
hydrocephalus.
**Translabyrinthine, retrosigmoid and middle fossa approaches are
possible, the latter options offering potential preservation of hearing in
smaller tumours with some intact function at presentation. ***In removing
larger tumours, it is often impossible to preserve hearing, or indeed facial
nerve function.
The appearances of a
meningioma in the left
cerebel- lopontine
angle (CPA), with a
coexisting vestibular
schwannoma in the
right CPA.

Question 18

Brain tumours in children

Answer 18

Brain tumours in children
Brain tumours are the most common solid tumours in children. Neonates
develop predominantly neuroectodermal tumours in supratentorial
locations,including subtypes detailed below
• teratoma;
• primitive neuroectodermal tumour (PNET);
• high grade astrocytoma;
• choroid plexus papilloma/carcinoma.
Older children tend to suffer infratentorial tumours, especially:
• medulloblastoma (an infratentorial PNET);
• ependymoma;
• pilocytic astrocytoma.

Question 19

Head injury
Air way assessment

Answer 19

Airway assessment
■ Ensure cervical spine immobilization
and check for vocal response
■ Clear mouth and airway if obvious
foreign bodies
■ Jaw trust and chin lift, if required
■ Consider airway adjuncts
■ If Glasgow Coma Score ≤8, consider
a definitive airway

Question 20

The primary survey in head injury

Answer 20

The primary survey in head injury
■ Ensure adequate oxygenation and
circulation
■ Check pupil size and response and
Glasgow Coma Score
as soon as possible
■ Check for focal neurological deficits
before intubation if
possible
■ Check blood sugar for hypoglycaemia

Question 21

Head injury
Pupils

Answer 21

Pupils
The pupil size should be recorded in millimetres, and
reactivity documented as present, sluggish or absent.
Uncal herniation can compress the third nerve,
compromising the parasympathetic supply to the
pupil, so that unopposed sympa- thetic activity
produces an enlarged and sluggish pupil, which then,
if the compression continues, becomes fixed and
dilated. However, an abnormal pupil size and
response may reflect pathology anywhere in the eye
or the reflex loop made up by the optic nerve, the
oculomotor nerve, and the brainstem.
Direct ocular trauma or
nerve injury in association
with a skull base fracture
can cause mydriasis (dilated
pupil) present from the time
of injury. Pre-existing
discrepancy in pupil size
(anisocoria), as a result of
Holmes-Adie pupil or
cataracts for example, may
also complicate assessment.

Question 22

Battle’s sign

Answer 22

Battle’s sign. A s k u l l b a s e
fracture may be associated with
bruising over the mastoid

Question 23

Head injury

Important aspects of injury

Answer 23

Important aspects of injury
Head injuries can be divided into three categories which over- lap and in which more
than one may be present in a patient.
**These are diffuse (the brain has been shaken),blunt (a direct non-penetrating blow)
and **penetrating (the cranium has been breached).
**Rapid deceleration often produces shearing of axons (diffuse axonal injury) and
**coup–contrecoup contusions.
**Penetrating injuries can be classified as low velocity or high velocity. The cavitation
caused by high velocity injuries is especially damaging to the brain.
**Skull fractures can be open or closed. If intracranial air can be seen on the x-ray, then
the dura has been breached too.
**Fractures may be linear (when they can be difficult to see on x-ray) or comminuted when
they may also be depressed.
**Fractured base of skull may present with bleeding from the eyes, ears nose or mouth or
with rhinorrhoea (CSF leaking from the nose).

Question 24

Classification of traumatic head injuries

Answer 24

Classification of traumatic head injuries
■ Scalp: open and closed (beware air under the dura)
■ Skull site: vault and base of skull
■ Skull type: linear, comminuted and depressed
■ Intracranial bleeding: extradural, subdural, subarachnoid
and intraparenchymal
■ Brain tissue causes: diffuse, blunt (direct, coup–contrecoup)
and penetrating

Question 25

MANAGEMENT OF MINOR AND MILD HEAD INJURY

Answer 25

MANAGEMENT OF MINOR AND MILD HEAD INJURY
In general, patients without on-going deficits can safely be dis- charged from the emergency department, provided they
meet the criteria listed below
An observation period of a few hours is advisable, especially where there is history of loss of consciousness at the time of
injury: this avoids discharge during the ‘lucid interval’ which may precede delayed deterioration due to an expanding
intracranial haematoma.
Discharge criteria in minor and mild head injury.
GCS 15/15 with no focal deficits
**Normal CT brain if indicated (see below)
**Patient not under the influence of alcohol or drugs
**Patient accompanied by a responsible adult
**Verbal and written head injury advice: seek medical attention if:
• Persistent/worsening headache despite analgesia
• Persistent vomiting
• Drowsiness
• Visual disturbance
• Limb weakness or numbness
**Patients who do not meet all the discharge criteria will need admission for a further period of observation, and in this
case it may be more economical to perform a CT to allow safe early discharge in this group.
National Institute for Health and Clinical Excellence (NICE) guidelines for
computed tomography (CT) in head injury.
**GCS <13 at any point
**GCS 13 or 14 at 2 hours
**Focal neurological deficit
**Suspected open, depressed or basal skull fracture
**More than one episode of vomiting
**Any patient with a mild head injury over the age of 65 years or
with a coagulopathy, for instance warfarin use, should be scanned urgently
**Dangerous mechanism or injury or antegrade amnesia >30 minutes
warrants CT within 8 hours

Question 26

SURGICAL ASPECTS OF HEAD INJURY

Answer 26

SURGICAL ASPECTS OF HEAD INJURY
Skull fractures
Closed linear fractures are managed conservatively, with primary
closure of associated wounds where possible.
**Skull base fractures may be complicated by CSF leak, pituitary
dysfunction, arterial dissection or cranial nerve deficits, with anosmia,
facial palsy or hearing loss typical. **Prophylactic antibiotics are not
usually required, even in the case of CSF leak, which generally resolves
spontaneously without the need for craniotomy and repair.
**Blind nasogastric tube placement is contraindicated in these patients.
**Fractures which involve the air sinuses may be managed as open
fractures, using broad spectrum antibiotics with or without exploration.
**Depressed skull fractures involve inward displacement
of a bone fragment by at least the thickness of the
skull .They occur when small objects hit the skull at high
velocity. They are usually compound (open) fractures, and
are associated with a high incidence of infection,
neurological deficit and late-onset epilepsy.
**Most compound fractures will require exploration,
debridement and elevation of the fragment. Prophylactic
treatment with a course of broad spectrum antibiotics is
normal practice

Question 27

Management of head injuries

Answer 27

Management of head injuries
■ Early discharge if NICE criteria are met
■ Scalp wounds need closure
■ Significant depressed fractures need elevating, antibiotics
and antiepileptics
■ Skull base fractures may may be associated with CSF
leak.
Pneumococcus vaccination is valuable, but prophylactic
antibiotics are not usually indicated

Question 28

Extradural haematoma

Answer 28

Extradural haematoma
**Extradural haematoma is a neurosurgical emergency. It results from
rupture of an artery, vein or venous sinus, in association with a skull
fracture.
**Typically, it is damage to the middle meningeal artery under the thin
temporal bone. A low energy injury mechanism, perhaps with brief loss of
consciousness, is sufficient to start the extradural bleeding. The patient may
then present in the subsequent lucid interval with headache, but without any
neurological deficit. At this stage, the increase in the intracranial volume is
not yet causing a significant rise in intracranial pressure because
compensation is occurring. However, once the limits of compensation have
been reached after as long as some hours rapid deterioration follows.
Extradural Heamatoma
**There is contralateral hemiparesis, reduced conscious level and ipsilateral
pupillary dilatation, the cardinal signs of brain compression and herniation
**On CT, extradural haematomas appear as a lentiform (lens- shaped or biconvex)
hyperdense lesion between skull and brain, constrained by the adherence of the
dura to the skull. Mass effect may be evident, with compression of surrounding brain
and mid- line shift. Areas of mixed density suggest active bleeding. A skull fracture
will usually be evident .
***Extradural haematoma requires immediate transfer to the most accessible
neurosurgical facility, for immediate evacuation in deteriorating or comatose patients
or those with large bleeds, and for close observation with serial imaging in all cases.
Overall mortality is around 10–20 per cent, but is considerably lower in isolated
extradural haematoma.

Question 29

Extradural haemorrhage

Answer 29

Extradural haemorrhage
■ Can occur in the context of apparently minor trauma
■ Isolated extradural haematoma may manifest as sudden
deterioration following a lucid interval
■ Lentiform lesion on computed tomography
■ Require immediate transfer to a neurosurgical unit for
decision on evacuation

Question 30

Acute subdural haematoma

Answer 30

Acute subdural haematoma
**Acute subdural bleeding arises from rupture of cortical vessels. In contrast
to extradural haematoma (and chronic subdural haematoma), acute subdural
haematoma is usually associated with a high energy injury mechanism and
significant primary brain injury. Conscious level is usually therefore impaired
at presentation, but may deteriorate further as the haematoma expands. Since
the dura is not adherent to the brain as it is to the skull, subdural blood is free
to expand across the brain surface giving a diffuse concave appearance
**Acute subdural bleeds of significant size or with significant associated
midline shift require evacuation, and the cumulative mortality in this group is
about 50 per cent. Smaller bleeds in neurologically stable patients may be
managed conservatively, with ICP monitoring, in a neurosurgical unit

Question 31

Chronic subdural haematoma

Answer 31

Chronic subdural haematoma
The epidemiology and presentation are completely different from
acute subdural haematoma. The patient is generally elderly, may
be taking antiplatelet or anticoagulant medications, and there is
usually a history of a recent fall, or falls. Cerebral atrophy
commonly found in the elderly is believed to stretch bridging
veins. These can then rupture after only minor trauma, bleed, and
then tamponade (stop bleeding due to the pressure which has
been produced by the bleed). Subsequent degradation of the
blood clot over days or weeks leads to osmotic expansion. It is
this which produces the mass effect.
Chronic Subdural Hematoma
**Presenting features, just as for any expanding
intracranial mass, include pressure symptoms, especially
headache and drowsiness, neurological deficit and seizures.
In this group, it is important to exclude coexisting electrolyte
disturbance and infections, which may be contributory.
**Imaging reveals diffuse hypodensity overlying the brain
surface. Recent bleeding may be isodense or hyperdense,
and mixed density can indicate an acute-on-chronic
subdural haematoma
Chronic Subdural Haematoma
**Drainage is performed using burr holes, often under local
anaesthetic (especially in elderly patients who present a substantial
anaesthetic risk).
**Urgency is dictated by the clinical condition of the patient. If clinically
stable, a delay of 7–10 days to allow platelet function to normalise after
withdrawal of aspirin may be considered.
**Anticoagulation should be reversed either by administration of
vitamin K, or urgently by transfusion of recombinant clotting factors in
patients who have deteriorated acutely.
**Occasionally, acute-on-chronic bleeds with residual solid clot or
septations require a craniotomy for adequate clot evacuation

Question 32

Subdural haemorrhage

Answer 32

Subdural haemorrhage
■ Relatively severe trauma
■ No lucid interval
■ Diffuse concave lesion on computed tomography
■ Require immediate transfer to a neurosurgical unit for
decision on evacuation
■ 50 per cent mortality
Chronic subdural haemorrhage
■ Occurs in the elderly, especially those on anticoagulants
■ May take days or weeks to develop
■ Diffuse hypodense lesion on computed tomography
■ Evacuation may be delayed until clotting has been improved

Question 33

Traumatic subarachnoid haemorrhage

Answer 33

Traumatic subarachnoid haemorrhage
Trauma is the most common cause of subarachnoid
haemorrhage and this is managed conservatively. It is
not usually associated with significant vasospasm, which
characterises aneurysmal subarachnoid haemorrhage .
***The possibility of spontaneous subarachnoid
haemorrhage actually leading to collapse and so causing
a head injury needs to be borne in mind and formal or CT
angiography may be required to exclude this

Question 34

Cerebral contusions

Answer 34

Cerebral contusions
**Contusions are common and are found predominantly where
the brain is in contact with the irregularly ridged inside of the skull,
i.e at the inferior frontal lobes and temporal poles. ‘
**Coup–contrecoup’ injury describes contusion of the brain on
the skull at the site of impact combined with contusion elsewhere
sustained as the brain rebounds from the initial impact.
**Contusions appear heterogenous on CT, reflecting their
composition of injured brain matter interspersed with acute blood .
**Contusions rarely require surgical intervention, but may
warrant delayed evacuation to reduce mass effect

Question 35

Diffuse axonal injury

Answer 35

Diffuse axonal injury
This is a form of primary brain injury, seen in the
high energy accidents, and which usually renders
the patient comatose. It is strictly a pathological
diagnosis made at post-mortem, but
haemorrhagic foci in the corpus callosum and
dorsolateral rostral brainstem on CT may be
suggestive, although the CT often appears normal.

Question 36

Arterial dissection

Answer 36

Arterial dissection
Cerebral arterial dissection occurs spontaneously or in the context of
trauma, which may be as trivial as nose-blowing or coughing. In the
hours after significant trauma, dissection of the carotid extracranially,
or at the skull base in association with fractures, is most common.
**It presents with headache, neck pain and focal ischaemic deficits,
due to occlusion by mural haematoma, thrombus and
thromboembolism.
**Intracranial dissection often affects the vertebral artery and may
result in subarachnoid bleeding
Arterial Dissection
**Development of a delayed deficit, especially in the
context of a skull base fracture involving the carotid
canal, should prompt urgent investigation and
treatment.
**Carotid dissection is generally managed with
anticoagulation, but vertebral dissection with
subarachnoid haemorrhage usually requires surgical
or endovascular intervention.

Question 37

Non-accidental injury

Answer 37

Non-accidental injury
Head injury in children and vulnerable adults may be due to abuse. Significant findings
include delayed presentation, injuries of disparate age, retinal haemorrhages, bilateral
chronic subdural haematomas, multiple skull fractures and neurological injury without
external signs of trauma
Types of brain injury
■ Apparent traumatic subarachnoid haemorrhage may actually be a spontaneous
subarachnoid haemorrhage which then led to the fall
■ Diffuse axonal injury results from high energy injury
■ Carotid dissection may be a delayed complication of skull
base fracture
■ Non-accidental injury in children: beware delayed
presentation
Ongoing management: prevention of secondary injury
**Following initial resuscitation and any emergency surgery
required for systemic pathology and intracranial haematomas,
the patient will require on-going management directed at
minimizing secondary brain injury.
**Unlike the primary injury which describes the diffuse axonal
injury and intracranial bleeding with which the patient presents,
secondary injury is often preventable through avoidance of
hypoxia and hypotension, and control of intracranial pressure.
Unchecked, secondary injury leads to a further cycle of
deterioration
Brain swelling and mass
lesions contribute to raised
intra- cranial pressure, which
compromises perfusion,
leading to secondary brain
injury and further swelling.

Question 38

Control of intracranial pressure

Answer 38

Control of intracranial pressure
**Intubation and ventilation is required early in the management of severe brain injury for airway control. It is
often required in moderate brain injury to facilitate the safe management and transfer of unstable and
frequently agitated patients and in order to control intracranial pressure.
**Sedating the patient prevents clinical assessment of intracranial pressure by monitoring of GCS and focal
neurological signs, leaving only pupil responses as a guide. It is therefore important that intracranial pressure
monitoring is instituted as soon as possible to guide pressure management. This is typically achieved using a
bolt ICP monitor, or else an external ventricular drain inserted into the lateral ventricle which also allows
drainage of CSF for pressure control.
**The patient will need measurements of coagulation parameters, platelet count, and CT head available prior
to insertion of the probe.
**A sustained rise of intracranial pressure over 20–25 mmHg is associated with a poor outcome, and
maintenance of a cerebral perfusion pressure of at least 60 mmHg is important in preventing secondary injury.
1. Initial measures
**Initial measures include positioning the head up 20–30° (reverse
Trendelenburg positioning by tilt of the whole bed if the spine has not been
cleared).
**The cervical collar should be loose enough so that it does not restrict
venous return.
**Ventilation is regulated to achieve normocapnia: hypocapnia may be used to
achieve transient ICP control in the short term, but the cerebral vasoconstriction
which results can produce hypoperfusion and eventual further secondary brain
injury.
**Sedation using a combination of opiates and barbiturates at escalating
doses and with boluses to coincide with turns and suctioning will assist in
control
2. Intermediate measures
**Where initial measures fail adequately to control ICP, sedation may be escalated and
supplemented with paralysis.
**External ventricular CSF drainage represents a useful adjunct to physiological
compensation.
**Mannitol can be administered to control ICP temporarily. This is helpful where there is
evidence of herniation, such as development of a dilated unresponsive pupil during
transfer. 100 mL of 20 per cent mannitol is a typical bolus. Repeated or excessive use is
counterproductive because it is an osmotic diuretic and produces hypovolaemia and
hypotension. This will compromise cerebral perfusion. Administration of mannitol
necessitates catheterising the patient to monitor fluid balance.
**Pyrexia increases brain oxygen requirements and cell damage, and so should be
avoided. Active induction of therapeutic hypothermia is effective in controlling intracranial
pressure, but predisposes to complications including sepsis and coagulopathy so that its
overall benefit is not firmly established.
3.Final measures
**Decompressive craniectomy involves removal of a portion of the
skull vault and opening of the underlying dura, so that brain swelling
can occur without the pressure increases predicted by the Monro
Kellie doctrine. Generally, a unilateral or bifrontal decompressive
craniectomy is performed, with the bone flap placed subcutaneously
in the abdomen, then replaced (cranioplasty) weeks or months later.
**An alternative strategy for managing uncontrolled intracranial
hypertension is induction of thiopentone coma. This carries a high
risk of complications and results in the loss of normal EEG activity and
pupil responses, compromising on- going evaluation of the patient.

Question 39

On-going management of significant head injury

Answer 39

On-going management of significant head injury
■ The patient should be intubated and ventilated with adequate
sedation and pressure monitoring
■ The goal of ongoing management is to minimise secondary
brain injury
■ Key parameters include oxygenation and ventilation, blood
pressure and ICP, and electrolyte balance. Pyrexia should be
actively controlled
■ A hierarchy of management strategies exists to achieve control
of intracranial pressure

Question 40

Pituitary dysfunction: endocrine and metabolic management

Answer 40

Pituitary dysfunction: endocrine and metabolic management
Electrolyte imbalance is common in TBI, and contributes to brain swelling
and to causing seizures. **Diverse mechanisms are involved. Cerebral salt
wasting, a poorly understood form of excretory dysregulation in association
with brain insult, leads to volume depletion and hyponatraemia.The
syndrome of inappropriate antidiuretic hormone (SIADH) leads to water
retention and hyponatraemia in the context of pituitary damage. This is of
particular concern in head injury since low serum osmotic pressure can
contribute to brain swelling, so hypotonic fluids are avoided in this setting.
**Conversely, antidiuretic hormone (ADH) secretion may be compromised in
the context of trauma, producing diabetes insipidus resulting in
hypernatraemia. This may be managed with boluses of desmopressin
All aspects of pituitary function may be compromised in the setting of TBI.
Routine screening of pituitary hormone levels is an important aspect of
optimal medical management.
Note that routine, rather than directed, administration of corticosteroids in
severe head injury is associated with increased mortality and is not
recommended.
Seizures
**Seizures may occur early (within 7 days) or late. 2 per cent (mild TBI) and
60 per cent (severe TBI with exacerbating features).
**Risk factors include injury severity, especially the presence of ICH, and
depressed skull fractures and tears of the dura.
**Antiepileptics, typically phenytoin, are administered prophylactically to
patients at high risk of seizures.
Nutrition
Enteral nutrition is preferred to intravenous parenteral nutrition on grounds of cost
and associated complications, and should be commenced within 72 hours of injury.
Prokinetics (e.g. metaclopramide, erythromycin) can be administered to promote
absorption
Investigations and prophylactic measures in significant head injury
■ Check pituitary function
■ Do not give hypotonic fluids
■ Monitor daily for electrolyte imbalance
■ Antiepileptics can be used prophylactically
■ Steroids should not be given routinely
■ Enteral nutrition should be started within 72 hours

Question 41

Head injury

Outcomes and sequelae

Answer 41

Outcomes and sequelae
1.Mild injury: concussion, second impact syndrome
and postconcussive syndrome
**Concussion is defined as alteration of consciousness as a result of closed head injury,
but is generally used in describing mild head injury without imaging abnormalities: loss of
consciousness at the time of injury is not a prerequisite.
**Key features include confusion and amnesia. The patient may be easily distractable,
forgetful, slow to interact or emotionally labile. Gait disturbance and incoordination may be
seen. It is proposed that in the context of disordered cerebral autoregulation, a second minor
injury may trigger a form of malignant cerebral oedema refractory to treatment.
**it should be considered in advice to individuals engaged in sports or activities carrying a
risk of further injury: symptomatic players should not return to play. After a very mild
concussion, they should not play again that day; after a severe concussion, they should
refrain for the rest of that season
Postconcussive syndrome is a loosely defined
constellation of symptoms, persisting for a prolonged
period after injury, Patients may report somatic
features, such as headache, dizziness and disorders
of hearing and vision. They may also suffer a variety
of neurocognitive and neuropsychological
disturbances, including difficulty with concentration
and recall, insomnia, emotional lability, fatigue,
depression and personality change.
2.Moderate and severe injury
**The long-term sequelae of significant brain injury are likely to
include many of the somatic and neurocognitive problems
described above, combined with the effect of deficits attributable
directly to the primary and secondary injury sustained.
**The Glasgow Outcome Score is used to quantify the degree of
recovery achieved after head injury
**Good recovery implies independence and potential to return
to work rather than a full return to previous capacity
Glasgow Outcome Score (GOS).
Good recovery 5
Moderate disability 4
Severe disability 3
Persistent vegetative state 2
Dead 1
Outcomes of a head injury
■ Post-concussion syndrome gives persisting headaches and problems in
concentrating
■ Players concussed when playing sport should not return immediately to the field
■ Good recovery is not necessarily a return to normal; it may be independent living

Question 42

Anesthesia
Definition
Stages

Answer 42

Anesthesia
state of pharmacologically
{
,
loss of consciousness
esthesia is a reversible
n General a
controlled sleep with reduction in cortical activity}. At sufficient anesthetic depth there is
absence of conscious awareness and recall, no sensory, motor or autonomic response to
stimulation.
Drugs made a patient unresponsive and unconscious , unable to feel pain and also
have amnesia .The drugs will be administered by anesthesiologist, a specially trained doctor
who will also monitor a patient’s vital signs and rate of breathing during the procedure.
Stages of general anesthesia
General anesthesia is similar to a comatose state and different from sleep.
this phase occurs between the administration of the drug and the loss of
Stage 1 (induction):
consciousness. The patient moves from analgesia without amnesia to analgesia with amnesia
wing a loss of consciousness, characterized by
the period follo
Stage 2 (excitement stage):
excited and delirious activity. Breathing and heart rate becomes erratic, and nausea, pupil
dilation and breath holding might occur. Because of irregular breathing and a risk of vomiting,
there is a real danger of choking; modern, fast-acting drugs aim to limit the time spent in stage
2 of anesthesia [most risky stage}so best to pass quickly.
muscles relax, vomiting stops and breathing is depressed. Eye
Stage 3 (surgical anesthesia):
movements slow and then cease. The patient is ready to be operated on.
too much medication has been administered, leading to brain stem or
Stage 4 (overdose):
medullary suppression; this results in respiratory and cardiovascular collapse.
The anesthetist’s priority is to take the patient to stage 3 of anesthesia as quickly as possible
and keep them there for the duration of the surgery.

Question 43

Anesthetic protocol include

Answer 43

Anesthetic protocol include

1-preanaesthesia {premedication}:analgesia ,sedation , antimuscarinic to dry secreations
,prevent vagal stimulation ,antiemetic,bronchodilator,h2 blocker.
2-induction of anesthesia best is mostly by iv
3-maintenance of anesthesia best is mostly by inhalational
4-skeletal muscle relaxation
5-analgesia’ as pre , during and post medication of surgery
6-other drugs: a-to reverse neuromuscular blockade b-to prevent vomiting c-to reverse
effects of opioids and benzodiazepine .

Question 44

The purpose of general anesthetic is to induce

Answer 44

The purpose of general anesthetic is to induce
-Analgesia - remove natural response to pain
-Amnesia - memory loss
-Immobility - removal of motor reflexes
-Unconsciousness
-Skeletal muscle relaxation

Question 45

Anesthesia

Types of medication

Answer 45

Types of medication
1-induction medications to produce unconsciousness
2-analgesics to produce pain relief
3-muscle relaxants
4-inhalational anesthetics to keep unconsciousness

Question 46

anesthetic drugs

Answer 46

anesthetic drugs

1-IV drugs
1-barbiturates and thiopentone ,used for induction and maintenance of anesthesia ,treatment
of status epilepticus ,reduce intracranial pressure ,contra indicated in porphyria and upper air
way obstruction.
2–propofol , drug of choice for day surgery where recovery is rapid used in ICU for sedation but
not children.
3-ketamine ,{unique in property that unlike other IV drugs ,it produces dissociative anesthesia
rather than depression of CNS ,intense analgesia with only superficial sleep},drug of choice in
patient with shock for emergency surgery ,avoided in patient with increased intracranial
pressure and high ocular pressure.
4-etomidate.
2-Inhalational drugs
Administered through face mask where IV is risky ,indicated in children, upper or lower air way
obstruction{isoflurane , sevoflurane , desflurane , enflurane ,ether, halothane and nitrous oxide
as a gas}.
Other drugs used
3-Muscle relaxants:- neuromuscular blocking agents act by blocking choline receptors
depolarizing agents like suxamethonium.
1
2.non depolarizing :-short acting{mivacurium},intermediate{atracurium},long
acting{pancuronium}.
Pharmacological blockade of neuromuscular transmission provides relaxation of muscles
allowing easy surgical access. Neuromuscular blocking agents are broadly classified into
depolarizing and non-depolarizing groups according to their mode of action. Suxamethonium is
the most commonly used depolarizing agent,widely used because of its quick onset and short
duration of action. These properties are useful where rapid endotracheal intubation is necessary
to protect the patient’s airway or short-duration surgery is performed.
Non-depolarising muscle relaxants provide longer, predictable activity, but require careful
monitoring, appropriate timing and reversal of their action by agents such as neostigmine at the
end of the procedure.
4-Opioids for analgesia ex, fentanyl
5-Benzodiazepines to relieve anxiety ex, midazolam

Question 47

Sequence of anaesthesia

Answer 47

: Sequence of anaesthesia
Induction
The most common technique now is
1- IV induction: drugs given intravenously in an appropriate dose, cause a rapid loss of
consciousness. Sodium thiopentone was commonly used until recently. Today propofol and
fentanyl or alfentanil are often used. Muscle relaxant is only given if the surgery cannot be
undertaken without paralysis, such as open abdominal surgery. Endotracheal tubes (ETs) can
also be used but generally require short-acting muscle relaxants and laryngoscopy for
intubation.
2-inhalational induction uses a volatile anaesthetic such as sevoflurane to induce anaesthesia
over 3-5min. Sevoflurane has superseded isoflurane, halothane and others as the agent of
choice for inhalational induction of anaesthesia .
Maintenance of anesthetic : can be done using continuous infusion of intravenous agent
(propofol) or inhaled vapour such as isoflurane, sevoflurane or desflurane..
Aims of GA during the maintenance period are:
-Controlled unconsciousness.
-Pain relief.
-Muscle relaxation.
-Reducing the response of the autonomic nervous system.
These are achieved with a combination of anaesthetics (IV and inhaled), opioids and muscle
relaxants.
Monitoring
During induction and maintenance of anaesthesia - clinical observations, supplemented by
The following equipment:-
-Pulse oximeter.
-Non-invasive blood pressure monitor.
-Electrocardiograph.
-Airway gases: oxygen, carbon dioxide and vapour.
-Airway pressure.
Clinical monitoring:
•
{ Capillary refill , Urine output : 0.5ml/kg – 1.5ml/kg/hr , Pulse volume , Skin temperature}
Why monitoring?
Disturbances can occur during surgery, they include
•
Airway obstruction, Respiratory depression, Apnea .
•
Cardiac depression, Arrhythmias, Bradycardia, Tachycardia.
•
Hypertension, Hypotension, Hypervolaemia , Hypovolaemia, Fluid shifts.
•
Hypothermia, Hyperthermia
The primary goal of Anesthesia is to keep the patient safe in the perioperative period.
Continuous monitoring of the patient during and after surgery allows early detection of
problems and correction
Even detection of equipment failure
Recovery
The time of recovery is a time of risk. All patients are observed by an anesthetist or recovery
nurse until they have regained airway control and cardiovascular stability and are able to
communicate .Patients are kept under clinical observation at all times and all measurements
recorded:
Level of consciousness.
Oxygen saturation and oxygen administration.
Blood pressure, respiratory rate, heart rate and rhythm.
Pain intensity .
IV infusions, drugs administered.
Other parameters (depending on circumstances) - ex, temperature, urinary output, central
venous pressure, end-tidal CO2, surgical drainage.
During recovery - clinical observations, supplemented by :-
-Pulse oximeter.
-Blood pressure monitor.
-The following must also be immediately available:
-Electrocardiograph.
-Nerve stimulator.
-Means of measuring temperature.
-Capnograph.
Complications
Complications of GA are varied and can be fatal but are rare
Damage to the mouth or pharynx, including damage to teeth and artificial crowns during
intubation
Minor allergic reaction to agents, producing nausea and vomiting (uncommon).
Major allergic reaction to agents, cardiovascular collapse, respiratory depression and jaundice
(uncommon).
Slow recovery from anesthetic due to poor cardiac, hepatic or renal function, drug interactions,
incorrect drug or dosage and inadequate reversal (uncommon).
Malignant hyperpyrexia caused by anesthetic gas or suxamethonium (rare).
Prolonged apnoea after suxamethonium caused by pseudocholinesterase deficiency (rare).
‘Awareness’ during surgery can occur when the patient is paralysed but without effective
anesthetic.
Because of the aim to give a fairly light anesthetic

Question 48

Side effects of general anesthesia include

Answer 48

Side effects of general anesthesia include
Confusion and memory loss - more common in the elderly, it is not necessarily permanent
Dizziness
Difficulty passing urine
Bruising or soreness from the IV drip
Nausea and vomiting
Shivering and feeling cold
Sore throat .
.
Special terms in anaesthesia:
●● Rapid sequence induction (RSI) is a technique that allows the airway to be rapidly secured. It
is used when there is a high risk of regurgitation that may lead to pulmonary aspiration
●● Total intravenous anaesthesia : (TIVA ) is becoming popular following the introduction of
propofol and the ultra-shortacting opioid remifentanil. The lack of a cumulative effect ,better
haemodynamic stability, excellent recovery. TIVA is routinely used in neurosurgery, airway laser
surgery, during cardiopulmonary bypass and for day-case anesthesia.
Management of airway during anesthesia Loss of muscle tone as a result of general anesthesia
means that the patient can no longer keep their airway open. Therefore, the patients need their
airway maintained for them. The use of muscle relaxants will mean that they will also be unable
to breathe for themselves and so will require artificial ventilation. Head tilt, chin lift and jaw
thrust manoeuvres, along with adjuncts such as oropharyngeal airways, are used to facilitate
bag-mask ventilation while induction agents exert full effect. Laryngeal mask airway or
endotracheal tube are then inserted and the patient is allowed to breathe spontaneously or is
ventilated during the procedure.
Complications of intubation
●● Failed intubation ●● Accidental bronchial intubation ●● Trauma to teeth, pharynx, larynx
●● Aspiration of gastric contents during intubation ●● Disconnection, blockage, kinking of tube
●● Delayed tracheal stenosis.

Question 49

Regional Anesthesia
Definition
Indications

Answer 49

Regional Anesthesia
An anesthesia affecting only large part of the body {anatomical part} produced by the
application of a chemical {local anesthetic} agent capable to provide reversible conduction block
of neural impulses associated with that part , subsequent recovery from the effect of the block is
spontaneous and complete without any evidence of nerve damage. Success of regional
anesthesia mostly depends on depositing the local anesthetic solution accurately on particular
space to block the specified nerves.
Indication
1.anesthesia
2.post operative analgesia
3.diagnosis and treatment of chronic pain syndromes
Regional anesthesia almost used for all kinds of lower abdominal ,perineal, urethral, rectal
,lower limb and orthopedic procedures. also can give {epidural type} analgesia through
epidural catheter to provide post operative pain relieve [for 3days to 1 week], during labor,
pancreatitis and pain of ischemic origin The treatment of benign chronic pain and cancer
pain by implanted epidural spinal catheter

Question 50

Local and regional anesthetic techniques

Answer 50

Local and regional anesthetic techniques
Local anesthetics can be used:
• topically to a mucous membrane, for example the eye or urethra.
• for subcutaneous infiltration.
• intravenously after the application of a tourniquet (IVRA).
• directly around nerves, for example the brachial plexus.
• in the extradural space (‘epidural anesthesia’).
• in the subarachnoid space (‘spinal anesthesia’).
The latter two techniques are more correctly called central neural blockade.

Question 51

The role of local and regional anesthesia:

Answer 51

The role of local and regional anesthesia:
• Analgesia or anesthesia is provided predominantly in the area required, thereby avoiding the
systemic effects of drugs.
• In patients with chronic respiratory disease, spontaneous ventilation can be preserved and
respiratory depressant drugs avoided.
• There is generally less disturbance of the control of coexisting systemic disease requiring
medical therapy, for example diabetes mellitus.
• The airway reflexes are preserved and in a patient with a full stomach, particularly due to
delayed gastric emptying (e.g. pregnancy), the risk of aspiration is reduced.
• Central neural blockade may improve access and facilitate surgery, for example by providing
profound muscle relaxation.
•Blood loss can be reduced with controlled hypotension.
• There is a considerable reduction in the equipment required and the cost of anesthesia. This
may be important in underdeveloped areas.
• When used in conjunction with general anesthesia, only sufficient anesthetic (inhalational or
IV) is required to maintain unconsciousness, with analgesia and muscle relaxation provided by
the regional technique.
• Some techniques can be continued postoperatively to provide pain relief, for example an
epidural.
• Complications after major surgery, particularly orthopedic surgery, are significantly reduced.
Whenever a local or regional anesthetic technique is used, facilities for resuscitation must
always be immediately available in order that allergic reactions and toxicity can be dealt with
effectively.
At a minimum this will include the following (facilities for resuscitation):-
• Equipment to maintain and secure the airway, give oxygen and provide ventilation.
• Intravenous cannula and a range of fluids.
• Drugs, including epinephrine, atropine, vasopressors and anticonvulsants.
• Suction.
•A surface for the patient that is capable of being tipped head-down.

Question 52

Epidural anesthesia

Answer 52

Epidural anesthesia
Epidural (extradural) anesthesia involves the deposition of a local anesthetic drug into the
potential space outside the dura. This space extends from the craniocervical junction at C1 to
the sacrococcygeal membrane, and anesthesia can theoretically be safely instituted at any level
in between. In practice, an epidural is sited adjacent to the nerve roots that supply the surgical
site; that is, the lumbar region is used for pelvic and lower limb surgery and the thoracic region
for abdominal surgery. A single injection of local anesthetic can be given, but more commonly a
catheter is inserted into the epidural space and either repeated injections or a constant infusion
of a local anesthetic drug is used. To aid identification of the epidural space, a technique termed
‘loss of resistance’ is used. The (Tuohy) needle is advanced until its tip is embedded within the
ligamentum flavum (yellow ligament). This blocks the tip and causes marked resistance to
attempted injection of either air or saline from a syringe attached to the needle. As the needle is
advanced further, the ligament is pierced , resistance disappears dramatically and air or saline is
injected easily. A plastic catheter is then inserted into the epidural space via the needle. The
catheter is marked at 5cm intervals to 20cm and at 1cm intervals between 5 and 15cm. If the
depth of the epidural space is noted, this allows the length of catheter in the space to be
determined.
Varying concentrations of local anesthetics are used depending on what effect is required. For
example, bupivacaine 0.5–0.75% will be needed for surgical anesthesia with muscle relaxation,
but only 0.1–0.2% for postoperative analgesia. Local anesthetic will spread from the level of
injection both up and down the epidural space.

Question 53

The extent of anesthesia is determined by:

Answer 53

The extent of anesthesia is determined by:
• The spinal level of insertion of the epidural. For a given volume, spread is greater in the
thoracic region than in the lumbar region.
• The volume of local anesthetic injected.
• Gravity: tipping the patient head-down encourages spread cranially, while head-up tends to
limit spread. The spread of anesthesia is described with reference to the limits of the
dermatomes affected; for example: the inguinal ligament, T12; the umbilicus, T10; and the
nipples, T4. An opioid is often given with the local anesthetic to improve the quality and
duration of analgesia, for example fentanyl.

Question 54

Spinal anesthesia

Answer 54

Spinal anesthesia
Spinal (intrathecal) anesthesia results from the injection of a local anesthetic drug directly into
the cerebrospinal fluid (CSF), within the subarachnoid space. The spinal needle can only be
inserted below the second lumbar and above the first sacral vertebrae; the upper limit is
determined by the termination of the spinal cord, and the lower limit by the fact that the sacral
vertebrae are fused and access becomes virtually impossible. A single injection of local
anesthetic is usually used, thereby limiting the duration of the technique. A fine, 22–29 gauge
needle with a ‘pencil point’ or tapered point (for example Whitacre or Sprotte needle) is used.
The small diameter and shape are an attempt to reduce the incidence of post dural puncture
headache. To aid passage of this needle through the skin and interspinous ligament, a short,
wide-bore needle is introduced initially and the spinal needle passed through its lumen.

Question 55

Factors influencing the spread of the local anesthetic drug within the CSF, and
hence the extent of anesthesia , include:

Answer 55

Factors influencing the spread of the local anesthetic drug within the CSF, and
hence the extent of anesthesia , include:
• Use of hyperbaric solutions (i.e. its specific gravity is greater than that of CSF), for example
‘heavy’ bupivacaine (0.5%). This is achieved by the addition of 8% dextrose. Posture is then used
to control spread.
• Positioning of the patient either during or after the injection. Maintenance of the sitting
position after injection results in a block of the low lumbar and sacral nerves. In the supine
position, the block will extend to the thoracic nerves around T5–6, the point of maximum
backwards curve (kyphosis) of the thoracic spine. Further extension can be obtained with a
head-down tilt.
• Increasing the dose (volume and/or concentration) of local anesthetic drug.
• The higher the placement of the spinal anesthetic in the lumbar region, the higher the level of
block obtained. Small doses of an opioid, for example morphine 0.1–0.25mg, may be injected
with the local anesthetic. This extends the duration of analgesia for up to 24h postoperatively.

Question 56

Monitoring during local and regional anesthesia

Answer 56

Monitoring during local and regional anesthesia
During epidural and spinal anesthesia, the guidelines on monitoring should be followed. A
conscious patient is not an excuse for inadequate monitoring! Particular attention must be paid
to the cardiovascular system as a result of the profound effects these techniques can have.
Maintenance of verbal contact with the patient is useful as it gives an indication of cerebral
perfusion. Early signs of inadequate cardiac output are complaints of nausea and faintness, and
subsequent vomiting. The first indication of extensive spread of anesthesia may be a complaint
of difficulty with breathing or numbness in the fingers. Clearly, these valuable signs and
symptoms will be lost if the patient is heavily sedated.

Question 57

Complications of central neural blockade

Answer 57

Complications of central neural blockade
These are usually mild and rarely cause any lasting morbidity. Those commonly seen
intraoperatively are due predominantly to the effects of the local anesthetic.
Hypotension and bradycardia
Anesthesia of the lumbar and thoracic nerves causes progressive sympathetic block, a reduction
in the peripheral resistance and venous return to the heart and fall in cardiac output. If the block
extends cranially beyond T5, the cardioaccelerator nerves are also blocked, and the unopposed
vagal tone results in a bradycardia. Small falls in blood pressure are tolerated and may be
helpful in reducing blood loss. If the blood pressure falls >25% of resting value, or the patient
becomes symptomatic , treatment consists of: • oxygen via a facemask; • IV fluids (crystalloids
or colloids) to increase venous return; • vasopressors to counteract the vasodilatation, either
ephedrine (3mg IV) or metaraminol (0.25mg IV); • atropine 0.5mg IV for a bradycardia.
Nausea and vomiting
These are most often the first indications of hypotension and cerebral hypoxia, but can also
result from vagal stimulation during upper abdominal surgery. If due to surgery, try to reduce
the degree of manipulation. If this is not possible then it may be necessary to convert to general
anesthesia. Atropine 0.3–0.6mg is frequently effective, particularly if there is a bradycardia.
Antiemetics can be tried (e.g. metoclopramide 10mg intravenously).
Postdural puncture headache
Caused by a persistent leak of CSF from the needle hole in the lumbar dura. The incidence is
greatest with large holes, that is, when a hole is made accidentally with a Tuohy needle, and
least after spinal anesthesia using fine needles (e.g. 26 gauge) with a pencil or tapered point
(<1%). Patients usually complain of a headache that is frontal or occipital, postural, worse when
standing and exacerbated by straining. The majority will resolve spontaneously. Persistent
headaches can be relieved (>90%) by injecting 20–30mL of the patient’s own venous blood into
the epidural space (epidural blood patch) under strict aseptic conditions.

Question 58

Contraindications to epidural and spinal anesthesia

Answer 58

Contraindications to epidural and spinal anesthesia
-Hypovolaemia: Either as a result of blood loss or dehydration. Such patients are likely to
experience severe falls in cardiac output as compensatory vasoconstriction is lost.
-A low, fixed cardiac output as seen with severe aortic or mitral stenosis. The reduced venous
return further reduces cardiac output, jeopardizing perfusion of vital organs.
-Local skin sepsis , risk of introducing infection.
-Coagulopathy , either as a result of a bleeding diathesis (e.g. haemophilia) or therapeutic
anticoagulation. This risks causing an epidural haematoma . There may also be a very small risk
in patients taking aspirin and associated drugs which reduce platelet activity. Where heparins
are used perioperatively to reduce the risk of deep venous thrombosis, these may be started
after the insertion of the epidural or spinal.
-Raised intracranial pressure , risk of precipitating coning.
-Known allergy to amide local anesthetic drugs.
-A patient who is totally uncooperative.
-Concurrent disease of the CNS, some would caution against the use of these techniques for fear
of being blamed for any subsequent deterioration.
-Previous spinal surgery or has abnormal spinal anatomy Although not an absolute
contraindication, epidural or spinal anesthesia may be technically difficult.

Question 59

Local anesthesia

SPECIFIC COMPLICATIONS

Answer 59

SPECIFIC COMPLICATIONS
- High epidural block extension due to an excessively large dose of local anesthetic in the
epidural space. It associates hypotension, sensory loss and difficulty breathing. In the most
severe cases it may require induction of general anesthesia and should be managed as an
emergency (securing of the airway and treatment of hypotension).
- Local anesthetic toxicity can occur early after injection when the catheter is advanced into
one of the many epidural veins. Aspirating prior to injecting local anesthetic is therefore
essential. Toxicity can also be delayed (20-40 min) if the total dose used is too large.
- Total spinal anesthesia occurring when the epidural needle or catheter is advanced into the
subarachnoid space. Then the local anesthetic is injected directly into the cerebrospinal fluid.
The action of local anesthetic on the brainstem associates hypotension, apnea, unconsciousness
and mydriasis.
- Epidural hematoma. Puncture of the numerous veins filling the epidural space may lead to the
development of a hematoma which can compress the spinal cord especially in patients with
coagulopathy or those receiving anticoagulants.
- Block failure explained by a catheter malposition (false loss of resistance during the procedure)
or by anatomic variation of the epidural space.