Category Archives: Surgical

Post operative ENT complications

Post adenoidectomy

Trickling blood behind uvula or hanging clot are reasons for re-exploration.

Post tonsillectomy

Secondary haemorrhage typically at 5-7 days.  Beware constant swallowing! White slough normal. Yellow (with pain) might mean infection so Corsodyl or peroxide gargles, 3-6x daily, possibly antibiotics.

History of bleeding but clear fossae – assess general condition and exclude bleeding disorder (family history), safety net.

If small clot, observe to see if enlarging. Every 15 mins or more if still spitting/swallowing. IV access and fast. Sit up.

Active bleeding needs anaesthetist for airway management, crossmatch too. Tonsil tray – adrenaline solution soaked swab applied to bleeding spot with Magill’s forceps until reaches theatre. Ice packs for back of neck. Post exploration NG tube to keep stomach empty.

Tranexamic acid, DDAVP? Eg vWD

Acute pancreatitis

Incidence increasing, approaching that of adults!? INSPPIRE international study. 

Diagnosis

Amylase 3x upper limit, radiology positive. 

Cullen’s and Grey Turner signs (umbilical and flank bruising respectively).

Amylase level not prognostic. False positive liver/renal impairment, GI inflammation.  False negative in 10%, esp drug induced!

Lipase more specific, only done in Huddersfield?! Stays high for longer.

Low calcium, high glucose seen.

Diagnosis mostly clinical. USS usually sensitive, else CT – more for complications (focal or diffuse enlargement, heterogeneous enhancement, irregular or shaggy outline, oedema of surrounding fat).

AXR may show sentinel loop, free gas (loss of psoas shadow). CXR for effusion.

Causes

I GET SMASHED

  • idiopathic (25% in children)
  • gall stones
  • ethanol
  • trauma
  • steroids – and other drugs, esp anti-epileptics, immunosuppressants eg azathioprine, cancer drugs.
  • mumps (even without parotitis), malignancy
  • autoimmune
  • scorpion sting!

But misses IBD, sepsis, Mycoplasma (early or late), genetic causes! 

Management

Prognosis good in children. Scoring systems in adults eg Modified Glasgow-Imrie not applicable, various paediatric versions, of debatable value. 

Fluid resuscitation then 1.5-2x maintenance requirements (not much evidence – don’t be afraid of positive balance! Keep urine output at 1ml/kg/hr), analgesia, early enteral nutrition if possible (to avoid bacterial translocation) else parenteral.

Antibiotics only for suspected sepsis.

Surgery eg necrosectomy. 

1/3 acute recurrent (defined as recurrence after full recovery). Often anatomical problems. Chronic associated with genetic disorders, metabolic, autoimmune.

ERCP for anatomical causes. Pancreatic enzymes. Non opiate pain management eg tricyclics. 

[NASPGHAN 2018 Guidelines]

Pyloric Stenosis

Pylorus is the name of the outflow tract of the stomach, the muscle in the wall controls how quickly the stomach empties.

For some reason, this muscle can become hypertrophied in the first month or two of life, to the point that the baby begins to vomit with feeds, become dehydrated and lose weight. Remains hungry of course, which may not be the case with some of the differentials.

The vomit is non-bilious of course, as the obstruction is above the bile duct.

4 male:1 female. Maternal history is more significant than paternal! NB Associated with TOF, other abnormalities. Associated with erythromycin use in infancy, particularly in first 14 days of life.

1st week to 5 months, but usually after 3 weeks.

Diagnosis

Peristalsis may be visible through abdominal wall. Olive shaped mass (2 cm diameter) felt RUQ just lateral to midline, under liver (sit on left side), after vomit.

When well established vomiting, hypochloraemic, hypokalaemic alkalosis characteristic (but not 100% specific).

On ultrasound scan, muscle thickness more than 3mm, transverse pyloric diameter more than 14mm (length similarly) – ie 3.14 (Pi, the mathematical constant)! [radiopaedia]

Differential diagnosis = reflux, sepsis, cow’s milk intolerance, other surgical condition eg malrotation, raised intracranial pressure, Congenital Adrenal Hyperplasia, biochemical imbalance eg renal tubular acidosis, inborn error of metabolism etc.

Treatment

Surgical pyloromyotomy (Ramstedt’s)- usually laparascopic. Quite a minor procedure, since the muscle is incised and then left to heal without any need to enter bowel itself or repair anything.

Penis problems

The foreskin cannot, and should not, be retracted in newborn babies.  It should gradually begin to separate in the first few years of life.

Recurrent balanitis leads to scarring around the meatus, so that you cannot see the slit opening of the penis itself.  In this case, the foreskin will balloon on passing urine (a minor degree of this can still be seen in children without scarring.

Can try application of topical steroid creams: 0.05% betamethasone cream should be used twice daily for 2 to 4 weeks.  Gently retract foreskin without causing any discomfort and apply a thick layer of cream to the tightest part of the foreskin.  Steroid creams of higher potency may be tried if this fails.

Circumcision if significant phimosis and steroid creams fail.

Smegma pearls

Retained smegma can accumulate into substantial but painless lumps down the shaft of the penis.  Can be ignored.

Balanitis Xerotica Obliterans

A form of lichen sclerosus affecting the tip of the penis, causing white, crinkly thickening.

Accidental Adrenaline self-injection

eg with Epipen or Emerade.

Causes vasoconstriction with potential for gangrene.

Try:

  • warm water immersion
  • local nitroglycerin paste
  • subcut infiltration with a mixture of 1.5mg of phentolamine, 1mL of 2% lidocaine (at site and along course of digital arteries)

[advised by National Poisons Information Service]

n=365 adrenaline injections to hand, 213 to digit.  No cases with clinically apparent systemic effects, only a few patients had ischemia. No patient was admitted or had surgery. [Annals of Emergency Medicine. 56(3):270-4, 2010 Sep. PMID: 20346537]

Central serous chorioretinopathy

Central serous chorioretinopathy (CSCR) = accumulation of subretinal fluid at the posterior pole of the fundus, ultimately leading to retinal detachment. Typically affects one eye only.  Vision becomes blurry and distorted, with objects often appearing smaller in the affected eye. May also cause difficulty with bright lights and contrast sensitivity.

Mechanism unknown, but associated with use of systemic corticosteroids, pregnancy, and Cushing’s syndrome.  Recently also been described after local corticosteroids including inhaled, intranasal, topical and periocular (!). Rare though.

Although blurred vision is a symptom of CSCR, it can be a side effect of periocular steroid treatment, as well as a symptom of whatever underlying eye condition is present (if any).

MHRA therefore says you should inform patients they should report any vision problems or disturbances.

[MHRA]

Idiopathic intracranial hypertension

Previously “Benign” Intracranial Hypertension but not entirely benign…

Intracranial hypertension but with normal CSF, and no ventriculomegaly. Presents with usual symptoms of early morning headache, effortless vomiting. VI nerve palsy may be seen, rarely II/IV. Papilloedema is often the first clue.

No sex differential prepubertally, not associated with obesity (contrary to popular belief).

Normal CSF opening pressure is 7.5cm of water <2yr, 13.5 <5yr, 20 over 5yr. Lumbar puncture is therapeutic; 2 step tap procedure is usually used if opening pressure is over 30cm. NB General anaesthetic can give false pos result! Secondary causes include drugs, endocrine conditions.

Since repeated LP is unpleasant, medical therapy can be considered. Topiramate is probably equivalent to the more usual acetazolamide (a diuretic). Steroids should be used for malignant hypertension (ie where there is rapid progression). Any of these treatments may result in a low pressure headache.

Surgical options include Optic nerve sheath fenestration, lumbar-peritoneal shunt.

Posterior urethral valves

1 in 5000 births.  Mostly failure of Wolffian duct development, rarely failure of urethral canalisation.

2/3 detected antenatally, with distended bladder. If missed, then present with urinary tract infection, abnormal voiding (dribble rather than fountain!) else incontinence (if toilet trained, of course).

Later detrusor failure, tubular dysfunction, renal failure.

Lymphoedema

In adults, usually after surgery or radiotherapy.  But can be primary, appearing in childhood (but not necessarily in early childhood).  Secondary causes include Klippel-Tranaunay, Noonans, Turners, other venous malformation.

The incidence of primary lymphoedema is approximately 1 in 6,000 births. Approximately 10 children are born each year with primary lymphoedema in Scotland.

Lymphoedema, particularly if not well controlled, “carries significant human, personal, financial and societal costs”. Apart from cosmetic issues, pain is often a significant problem (underestimated), plus risk of cellulitis.  Inadequate treatment increases risk of complications:

  • fibrosis,
  • papillomatosis (warty growths consisting of dilated lymphatics and fibrous tissue)
  • lymphorrhoea (leakage of lymph fluid through the skin),
  • functional limitations
  • psychological morbidity, social isolation and limitation of life choices, including employment opportunities

So early diagnosis and control important.

Examination

Deep pressure for at least 30 seconds! If pits, then lymphatics ok.

Positive Stemmer sign= the inability to pick up a fold of skin at the base of the second toe, indicating thickening of the skin. This is useful in differentiating lymphoedema from other forms of oedema. [http://www.woundsinternational.com/ Journal of Lymphoedema, 2009, Vol 4, No 2]

Investigations

Consider secondary causes, as above.

Consider LFTs, thyroid function (impaired lymphatic drainage seen in hypothyroidism, hence oedema and even effusions).

Imaging to assess venous blood flow eg USS with dopplers.

MRI can show hypertrophy of fat, as in lipoedema (see below), or other tissues (viz Klippel Trenaunay).

Lymphoscintigraphy is gold standard but not readily available.

Differential is Lipoedema – almost exclusively females, presents at or after puberty, symmetrical lower limb enlargement.  Often a history of easy bruising and tenderness in the affected limbs. Lymphoedema can later develop as a secondary complication.

Further advice from http://www.thebls.com/patients/index.php?bls_user=9f0a85c93b84f4e36a2629f6d17c38e7

Patient support from http://www.lymphoedema.org/

[SMASAC Short Life Working Group on Lymphoedema – Lymphoedema Care in Scotland, Achieving Equity and Quality, 2013]

 

Head injury

In minor head injury (definition?!), statistically significant correlation between intracranial haemorrhage and:

  • skull fracture
  • focal neurology
  • history of loss of consciousness
  • GCS abnormality (difficult to gauge in preverbal children…)

Headache and vomiting were not found to be predictive and there was great variability in the predictive ability of seizures. (meta-analysis, ArchDisChild 2004;89)

SIGN 110 suggests immediate CT for:

  • GCS less than 14
  • high speed mechanism
  • witnessed loss of consciousness for more than 5 minutes
  • Suspicion of open or depressed skull fracture
  • Any sign of basal skull fracture
  • Tense fontanelle
  • Focal neurological deficit

Otherwise, early (ie within 8 hours) CT should be considered if:

  • bruise/swelling/laceration >5cm on head
  • post-traumatic seizure without epilepsy (and not reflex anoxic)
  • amnesia (antero- or retrograde) >5 minutes
  • suspicion of NAI
  • Significant fall
  • 3+ discrete episodes of vomiting
  • abnormal drowsiness
  • GCS other than 15 in under 1yr old, assessed by experienced provider

If suspicion of NAI, extra rule applies – CT should be done “as soon as child is stable” (and ideally within 24 hrs) if under 1 yr, or neuro signs (incl haemorrhagic retinopathy).

Any loss of consciousness should be assessed, but interestingly retrograde amnesia has to be for >30 minutes to warrant assessment, whereas NICE would do immediate CT! Otherwise 2+ vomits, severe and persistent headache, coagulopathy, difficulties with assessment or social situation, or any other indication for CT.

Admit if any indications for CT, although it also says discharge can be considered if social situation suitable!

NICE head injury (2017) guidelines

similar criteria, but suggests immediate CT for more. Change in practice from admit and watch (Royal College of Surgeons guidelines) to diagnose and decide. Leads to far fewer skull XRs, a lot more CTs and maybe half as many admissions. Some centres have seen cost savings due to earlier discharge.

CT within 1 hour for:

  • age over 1 year, GCS<14 on initial assessment;
  • age under 1 yr; GCS<15 on initial assessment.
  • GCS<15 at 2 hours after injury.
  • age under 1yr plus bruise, swelling or 5cm laceration.
  • Suspicion of NAI.
  • Loss of consciousness >5min (witnessed).
  • Post-traumatic seizure without epilepsy.
  • Abnormal drowsiness.
  • Suspected open or depressed skull fracture, or tense fontanelle.
  • Any sign of basal skull fracture – haemotympanum, panda eyes, CSF leak from ears/nose, Battle’s sign.
  • Focal deficit.

Plus CT within 1 hour if MORE than 1 of the following:

  • Witnessed loss of consciousness more than 5 minutes
  • Abnormal drowsiness
  • 3+ discrete episodes of vomiting
  • Dangerous mechanism eg high speed road traffic accident, fall >3m, high speed projectile
  • Amnesia (retro or antegrade) >5 min

If only 1 of the above, then observe minimum 4 hours – go to CT if during that time:

  • GCS <15
  • Further vomiting
  • Episode of abnormal drowsiness

In children under 10yr, CT for spine should be avoided (risk to thyroid) unless severe head injury (eg GCS<=8), strong suspicion despite plain films, or inadequate plain films. Over 10yr, CT is investigation of choice if:

  • GCS<13 (so 1 point less than for head).
  • intubated.
  • inadequate plain films.
  • Continued suspicion.
  • Needing multi-region scan anyway!

Neuroscience centres are expected to be able to perform initial management of multiple injuries in children. Local guidelines for transfer should be drawn up – there are benefits for being in a neurosurgical centre even if surgery is not required.

Kids with a fracture are not as prone to intracranial lesions as adults, at the same time they are more likely to have intracranial lesion without a fracture!

Note increased risk of malignancy with CT.  So observe for 4 hours if persistent vomiting, review by senior clinician to decide further observation rather than CT. Involve parents in decision [BMJ 2019;365:l1875]

Management

No good RCTs! Avoid secondary brain injury – 1 episode hypotension post head injury triples mortality. Cerebral blood flow is low in first 24hr, peaks at 48hr. Depends on temperature, seizures, pain/anxiety.

Glasgow Coma Score (GCS) 9-12 is moderate, <=8 is severe (equivalent to P or U in AVPU score) and is indication for ventilation to protect airway as reflexes potentially unreliable.

Diffuse axonal injury progresses over 24+ hrs, difficult to see on scan.

Consider external drain/ventriculostomy for intracranial haemorrhage. ?Remove contused brain ?Decompressive craniectomy

Neuroprotective strategy:

  • Head up 30deg, straight
  • Maintain pCO2 at 35-40mmHg
  • Cool if febrile (awaiting data on role of hypothermia). Paralyse to avoid shivering. Paralysis will make seizures difficult to recognise: role for prophylactic anti-epileptics?
  • Analgesia
  • (steroids not helpful)
  • CVP&arterial BP monitoring, ensure adequate perfusion pressure
  • ICP monitoring if neuro signs, GCS <9, post decompression. Bolt gives data but does not allow CSF drainage. ICP takes 7-10 days to settle

For RICP, 3% NaCl 3-5ml/kg bolus – Keep osmo <310mmol/l.

For induction, thiopentone is traditionally used. Ketamine theoretically increases ICP but no real evidence. Adding fentanyl smooths cardiovascular response to procedure.

CT@72h is prognostic.

Shaken Baby: lethargy, vomiting, apnoeas, seizures (40-80%), opisthotonus, irritability. See NAI.