Assessment and Management Of Airway Burns

The term “inhalational injury” has been used to describe the aspiration of toxic products of combustion, but also more generally any pulmonary insult associated with a burn injury. Patients with cutaneous burns are two to three times more likely to die if they also have lower airway burns. Death may be a direct result of lung injury but is usually due to the systemic consequences of such injury. It may be impossible to distinguish lung injury caused at the time of the burn directly to the lungs by a burn from injury due to the systemic consequences of the burn. Inhalation injury, age, and burn size are the three most commonly cited predictive factors for prolonged ventilator dependence, hospital stay, and death in burn patients. The injuries can generally be divided into three classes:
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).

In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).

Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.

Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.

Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed

Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response

The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.

Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding

There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.

Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.

Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.

Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.

Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.

Critical Care/Medical Sites of Interest

Hi everyone, I am trying to collect and make list of all useful websites in CRITICAL CARE. Here is the beginning and if you know some, please share for benefit of all.

Critical Care Medicine
http://www.ccmtutorials.com
http://www.aic.cuhk.edu.hk/web8/index.htm
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/index.htm
http://www.uihealthcare.com/vh/
http://cim.ucdavis.edu/
http://www.thoracic.org/sections/clinical-information/critical-care/index.html
http://www.anzics.com.au/
http://www.lhsc.on.ca/programs/critcare/pge/
http://www.dicm.co.uk/papers.htm - Great UK based website, primarily for those doing the UK DICM but a treasure trove of evidence for any intensivist

Evidence Based Medicine
http://www.ebmny.org/">http://www.ebmny.org/">http://www.ebmny.org/
http://www.cche.net/usersguides/ebm.asp
http://www.cebm.utoronto.ca/
http://www.cebm.net/

Anesthesia
http://www.virtual-anaesthesia-textbook.com/vat/main.shtml

Acid Base
Acid Base Tutorial - http://www.acid-base.com/
Acid Base Physiology - http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php

Mechanical Ventilation
http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm
http://www.aic.cuhk.edu.hk/web8/mech%20vent%20intro.htm

Sepsis
http://www.sepsisforum.org/">http://www.sepsisforum.org/">http://www.sepsisforum.org/
http://www.elililly.com/
http://www.ardsfoundation.com/
http://ssc.sccm.org/
http://www.ardsnet.org/

Radiology
http://www.learningradiology.com/
http://www.anatomyatlases.org/

Chest XRay
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr.htm
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/atlas/cxratlas_f.htm
http://www.learningradiology.com/lectures/facultylectures/BASIC%20CXR-mod-Adam_files/v3_document.htm
http://www.usfca.edu/fac-staff/ritter/chestxra.htm

Trauma
http://www.trauma.org/

Pupil assessment
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm

Delirium
http://www.icudelirium.org/delirium/CAM-ICUTraining.html

Anatomy
http://www.pbs.org/wnet/brain/3d/
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/anatomy.htm
http://msjensen.cehd.umn.edu/webanatomy/
http://www.imaios.com/en/e-Anatomy

IABP
http://www.aic.cuhk.edu.hk/web8/IABP%20pressure%20waveforms.htm

ECHO
http://www.criticalecho.com (By Kishore CMC Vellore)

Brain Herniation
http://rad.usuhs.mil/rad/herniation

Assessment for extubation

Despite advances in mechanical ventilation and respiratory support, the science of determining if the patient is ready for extubation is still very imprecise. A lot depends on the clinician’s threshold for reduction in ventilatory support, than does the modes of ventilatory wean.

Patients who can be extubated safely can be divided into three phases-
1. Freedom from the primary problem that prompted mechanical ventilation
2. Identifying whether the patient will sustain spontaneous respiration and ventilation and also when the patient is failing the assessment
3. What to look for immediately before extubation.

These assessments are multifaceted and usually include the overall patient condition, hemodynamic stability, neurological and muscular status and adequacy of gas exchange.

Commonly used clinical parameters that predict successful weaning from
mechanical ventilation.

Parameter with Desired value
Respiratory rate Less than 30-38 breaths/minute
Tidal volume 4-6 mL/kg
Minute ventilation 10-15 L/minute
Negative inspiratory force -20 to –30 cm H2O
Maximal inspiratory pressure (MIP) -15 to –30 cm H2O
Mouth occlusion pressure 100 msec after the
onset of inspiratory effort (P0.1) divided by MIP 0.3
Rapid shallow breathing index (RSBI)
(respiratory rate divided by tidal volume) 60-105
Rapid shallow breathing index rate
[(RSBI2 – RSBI1)/RSBI1] x 100 Less than 20%
CROP score (an index including compliance,
rate, oxygenation and pressure) 13
PaO2/FiO2 ratio >150-200
Despite high sensitivity, however, these parameters lack specificity.

All the patients who are deemed fit for extubation should undergo some means of assessment to see if they will tolerate extubation. It is routine to perform Spontaneous breathing trial (SBT), by means of – CPAP of 5 cm of H2O, T –Piece trial, or Pressure support of 7 cm of H2O. Once the patient is on SBT we should watch for indicators of failure, which are –

1. Inadequate gas exchange
Arterial oxygenation saturation (SaO2) <85% - 90% PaO2 <50 – 60 mmHg pH < 7.32 Increase in PaCO2 >10 mmHg

2. Unstable ventilatory/respiratory pattern
Respiratory rate >30 – 35 breaths/minute
Respiratory rate change over 50%

3. Hemodynamic instability
Heart rate >120 – 140 beats/minute
Heart rate change greater than 20%
Systolic blood pressure >180 mmHg or <90 mmHg Blood pressure change greater than 20% Vasopressors required 4. Change in mental status
Agitation
Anxiety
Somnolence
Coma

5. Signs of increased work of breathing
Nasal flaring
Paradoxical breathing movements
Use of accessory respiratory muscles

6. Onset of worsening discomfort ± diaphoresis

Another parameter that is widely used is the Rapid shallow breathing index (RSBI), from which we can calculate the RSBI rate which is the measure of change of RSBI over time, and may offer more predictive value .A RSBI rate of less than 20% is 90 % sensitive and 100% specific for predicting weaning success .It has a positive predictive value of 100% and negative predictive value of over 81 %.

Finally, once it is confirmed that patient can sustain spontaneous breathing , we can extubate the patient provided—
1 .Presence of a patent airway –assessed with “Cuff leak test”( dividing expiratory volume by inspiratory volume and multiplying with 100)
2. Patients’ ability to consistently protect the airway and clear secretions –assessed by the presence of adequate cough and gag reflex.
3. Mental status compatible with maintenance of airway and secretion clearance.
4. Absence of any other reasons for potential post-extubation failure—
- severe pain
- presence of apnea
- poorly controlled seizures
- risk of massive upper GI bleeding.

Thanks to Dr Harjit Mahay for contributing this wonderful article.

Croup Vs Epiglotitis

Croup-Acute Laryngotracheobronchitis: inflammation of the glottic & subglottic region (narrowest part)

1. Viral Croup - parainfluenzae viruses
- occasionally RSV, rhinoviruses, or measles
- coryzal prodrome, low grade fever
- rare < 6/12, consider ? underlying lesion - commonest obstruction at 6/12 to 6 yrs - median age of presentation 18/12 - more common in autumn & winter - <5% require intubation 2. Spasmodic Croup - children with an allergic nature
-? spectrum of asthmatic population
- no coryzal prodrome / fever

3. Bacterial Tracheitis - usually Staph. aureus ± H. influenzae, group A Strep.
- high fever, WCC, purulent secretions
-* risk of sudden obstruction

Varied Clinical Presentation
a. signs of mild croup
- URTI preceding 2-3 days
- loud barking "croupy" cough
- gradual onset inspiratory stridor which is high pitched
- hoarse voice
- no postural preference
- mild fever
- often a past history of croup

b. moderate
- stridor on inspiration & expiration
- tachypnoea
- flaring alar nasae
- suprasternal/intercostal retractions

c. severe - restlessness caused by hypoxia
- exhaustion & listlessness
- deteriorating conscious state
- cyanosis on air

Differential diagnosis
- epiglottitis
- aspiration of foreign body
- bacterial tracheitis
- retropharyngeal abscess
- peritonsillar abscess

Diagnosis
i. history and examination * mainstay of diagnosis
ii. radiology of the larynx (ESS or ICU) ®
"steeple" sign - AP view
widened hypopharynx - lat. view, only ~ 40-50% of cases
iii. direct laryngoscopy under GA

Management
a. minimal disturbance - VM & VO2,nursed by parent
b. adequate hydration,but propensity for pulmonary oedema; hypo-Na+ & convulsions have occurred 2° to SIADH with airway obstruction
c. oxygen therapy ® SpO2 > 90%- hypoxia from parenchymal infection ± increased interstitial water
d. humidification - mainstay for years but studies showing efficacy are lacking now abandoned by many centres but anecdotal evidence ? otherwise
e. steroids - dexamethasone ~ 0.6 mg/kg (= 12 mg) stat., then 0.15 mg/kg q6h.
Given on admission - decreases intubation rate & duration of stay
Failed extubation rate - administer 24 hrs pre & 12 hrs post-extubation
May also be of use in spasmodic croup
f. nebulized adrenaline - 1:1,000 ~ 0.5 ml/kg £ 5 ml of 0.1% solution, nebulised 2 hrly, this dose is effective, has little systemic effect, and is less than the recommended dose for the racemic solution -subsequent doses ® less effective. The obstruction may be more severe after the effect has worn-off ® rebound phenomenon ? progression of the disease process.
-In Acute LTB - lasts ~ 1-2 hrs,doesn't alter course but may allow secretion expectoration and prior to intubation, enhances induction
-In spasmodic croup - may obviate need for intubation
- Post ETT / endoscopy oedema where effect is often dramatic
- prior to transfer if not for intubation
- prior to anaesthesia & intubation if tolerated
g. Antibiotics - only for proven bacterial infection
h. Intubation ~ 2-5% of cases, nasotracheal,use 1 mm less than "size for age"

Indications for Intubation NB: essentially subjective assessment
a. ­ respiratory rate, HR, and chest wall retractions
b. cyanosis not responsive to oxygen
c. exhaustion and/or confusion
d. increased use of, and failure to respond to, nebulised adrenaline
e. need for transport to another hospital

Method
-spontaneously breathing,
-inhalational anaesthetic induction is prolonged
-ETT ~ 1 size smaller for age to minimise trauma
-most safely passed orally, then changed to a nasal
-small tubes are shorter and may be difficult to secure
-sedation ± arm splints to prevent self extubation
-stomach should be emptied with a nasogastric tube
-CPAP or IPPV with PEEP to maintain oxygenation
- size limited to > 3.0 mm, due to requirement to pass a suction catheter to clear secretions

Extubation
-can be attempted when a leak is present with positive pressure or coughing,
- or when the disease has run its course at 5 to 7 days
Reintubation may be required, but the incidence is reduced by administration of steroids prior to extubation ® prednisolone ~ 2 mg/kg/day.
Prior to steroid therapy intubation duration was average 5 days, but now reduced to 2-3 days.

Bacterial Tracheitis
-results in purulent secretions, pseudomembranes and ulceration of epithelium within the trachea
-death can result from upper airway obstruction, endotracheal tube blockage, and toxic shock
-either a primary bacterial infection or a superinfection on primary viral illness
-the causative organisms are,
a. Staphylococcus aureus
b. Haemophilus influenza type B
c. Streptococcus pneumoniae
d. Branhamella catarrhalis

Clinical Presentation
a. fever & toxaemia
b. respiratory distress
c. similar to epiglottitis except for
- the presence of a cough
- a subjective difference in quality of the stridor

Diagnosis
i. CXR - may show tracheal membranes
- narrowing & "fuzziness" are variable
ii. ETT - absence of epiglotitis
- suction following intubation ® pus and membranes in the trachea

Management - similar to that for epiglottitis (see over)
- if intubation is required, the ETT may block acutely with secretions ® aggressive tracheal suction ± reintubation
- bronchoscopy to clear tracheal pus should be considered where the airway remains compromised after intubation, suction and reintubation
- initially, there may not be a leak around an appropriately sized endotracheal tube
- sputum should be sent for gram stain and culture, and urine for rapid antigen identification
- extubation is best performed when, the fever and secretions have settled, and a leak is present around the endotracheal tube
- initial antibiotic therapy ® cefotaxime ~ 50 mg/kg q6h for 10/7, then by MC&S

Epiglottitis: supraglottic, infective inflammatory lesion, caused almost exclusively by Haemophilus influenzae - type B ± occasionally streptococci, staphlococci, or pneumococci
a. acute onset - short history (hrs) with no preceding URTI
b. high fever & toxaemia
c. stridor - low pitched, inspiratory ± expiratory snore, usually constant in nature
d. absence of cough and reluctance to talk
e. characteristic posture - sitting forward,mouth open, drooling & dysphagia
f. diagnosis
- direct laryngoscopy
- urine latex antigen agglutination
- ~ 80% blood culture (+)'ve
- lateral XRay ® "thumb print"

Most commonly children from 2 to 7 years but the disease can involve adults and infants due to septicaemia. The severity of the illness is often out of proportion to the airway obstruction.Children less than 2 years of age may present with airway obstruction atypically accompanied by apnoea, URTI, low grade fever, and/or cough and sudden total obstruction may be precipitated by,
a. instrumentation of the pharynx
b. painful stimuli - eg. IV insertion
c. supine posture

Management
a. minimal disturbance - nurse in mothers arms, etc.
b. ready access to intubation equipment
c. oxygenation - mask or nasal cannulae, if obstructs ® CPAP/assist by bag
d. antibiotics
- cefotaxime ~ 50 mg/kg q6h ± chloramphenacol ~ 25 mg/kg q6h or
- ampicillin was used but high percentage of resistant strains
e. intubation - all but the mildest cases, average duration ~ 18 hours but may be required for longer in cases with,
- pulmonary oedema
- pneumonia
- cerebral hypoxia
f. racemic adrenaline is of no use in this condition and can precipitate obstruction

Epiglottitis - Intubation Indications
1. severe or progressive respiratory distress
2. prior to transportation to a tertiary centre
3. following diagnosis by direct laryngoscopy under GA

- Patients can be managed without intubation if they remain in an area where appropriate personnel, equipment and supervision is available. Such patients are generally older, co-operative and are seen early in the day with minimal signs of obstruction. Diagnosis in these cases is made by lateral neck XRay
- An IV line can be inserted before anaesthesia, but should be delayed until after induction when the patient is distressed or obstruction is severe in order to avoid sudden obstruction.
- In spontaneously breathing, inhalational GA is best tolerated in the sitting position.
- Agitation and distress at induction may be due to acute hypoxia.
- The patient can be laid flat on loss of awareness, and airway obstruction overcome by application of CPAP or assisted ventilation.
- Laryngospasm may be precipitated if laryngeal stimulation occurs prior to surgical anaesthesia being achieved.
- Copious and persistent pulmonary oedema fluid may obscure the larynx, making intubation difficult.
- An ETT of normal size for age or one size smaller should be inserted orally then changed to the nasal route once the child has settled
- Positive pressure should demonstrate a leak around the tube.
- The patient can be sedated ± restrained to prevent self-extubation.
- Muscle relaxants are not routinely required unless IPPV/PEEP is required to overcome hypoxia and hypoventilation from pulmonary oedema.

Complications
a. respiratory failure / obstruction
b. pulmonary oedema ~ 7-10% of cases and is precipitated by intubation
- hypoxia & SNS discharge - ­ PAP
- vascular - endothelial injury & capillary permeability
- decreased intrathoracic pressure after intubation, augmenting venous return, and increasing transmural pulmonary vascular hydrostatic pressure gradients
c. barotrauma
- pulmonary interstitial emphysema (PIE)
- pneumothorax
- pneumomediastinum
d. septicaemia / pneumonia

Extubation Criteria
a. when the fever has settled
b. signs of inflammation subside ® usually ~ 18 hours
- pain subsided
- able to swallow
- free movement of the larynx

NB: exceptions are where hypoxia and reduced lung compliance persist direct laryngoscopy prior to extubation is not required

Thanks to Dr Anuj Clerk for this wonderful article.

Perioperative management of the patient with pheochromocytoma

The KEY: Communication between surgeon, anesthesiologist, and internist.

Background:
Pheochromocytoma is an uncommon neuroendocrine tumor of the chromaffin cell.
The most common sign of the tumor is hypertension, which can be paroxysmal.
The tumor’s intermittent catecholamine surges can cause a variety of symptoms,including headache, chest pain, palpitations, diaphoresis, dyspnea, anxiety,and dizziness.

Surgical excision can prevent the life-threatening complications of hypertensive crises, stroke, arrhythmias, and myocardial infarction.Before 1961,surgical mortality ranged from 24–45%. With appropriate medical preparation and an experienced anesthesiologist and surgical team, survival of excision of a pheochromocytoma is 93.3–100%

Preoperative preparation
Catecholamine excess causes --vasoconstriction that leads to both hypertension and hypovolemia.
Pheochromocytoma patients can die intraoperatively from--severe hypertensive crisis or hypotension that leads to cardiovascular collapse.

When tumor veins are ligated during surgery, the sudden drop in circulating catecholamines can lead to vasodilatation. The catecholamine output of the contralateral adrenal may be suppressed from previous catecholamine excess. In the hypovolemic patient, this can lead to hypotension, shock, and death.

Alpha adrenergic blockade is the cornerstone of preoperative preparation
-it treats both hypertension and vasoconstriction
-improves circulating plasma volume prior to surgery.

Phenoxybenzamine[Non selective, non competitive]-start 2 weeks prior to Sx 5-10 mg BID, step up to control BP~140/90 with max. 300 mg per day. Caution Postural hypotension, nasal stuffiness, reflex tachycardia.

Selective Alfa 1 blockers[Prazosin SR 2-20 mg BD ,doxazosin 1-16 mg OD]- do not block NA re uptake- less reflex tachycardia and orthostatic hypotension so better tolerated.

Liberalization of salt in the diet along with alpha blockade should expand plasma volume.

Beta blockade: Propanolol/Atenolol/metoprolol few days after Alfa Blockade[once reflex tachycardia noted] but few days before srgery.[if not contraindicated by heart failure or asthma]. Beta-blockers may also prevent perioperative arrhythmias and cardiac complications.

As calcium ion transport is essential for release of catecholamines from chromaffin cells, calcium channel blockers are used for control of blood pressure and preoperative preparation at some centers Less periop fluid requirement and post op hypotension in one French study.

Metyrosin [(alpha-methyl-p-tyrosine)Tyrosin hydroxylase inhibitor] reserved for refractory cases at doses of 1–4 mg per day -Very Toxic no longer used

Preoperative evaluation of myocardial function MUST.[left ventricular hypertrophy and dysfunction, but chronic catecholamine excess induced cardiomyopathy.]

Pre op Target:
24 BP monitoring, all readings <160/90, HR <100/min, Postural drop in BP with compensatory tachy as sign of adequate alfa blockade. Intraoperative Management:
-Avoid Histamine release causing agents during induction eg. Morphine
-Adrenaline followed by noradrenaline infusion for fluid refractory hypotension [CVP~10-15mmHg].
-Terlipressin 1 mg followed by vasopressin infused can be used.
-Na.nitroprusside infusion better then Phentolamine boluses [due to shorter duration of action] for hypertensive episodes.
-IV Nicardipine and Magnesium can be used to control hypertensive spikes.
-Betablockers for tachyarrhythmia.

Postoperative Management
-12-24 hours HDU/ICU care must.
-patient may remain hypertensive up to 2 weeks after excision.
-urinary catecholamines should be checked to ensure no additional tumor remains.
-hypoglycemia may develop and persist into the postoperative period once the tumor is removed[Catecholamine withdrawal + Beta blockade induced limit to compensation and unawareness]. Glucose should be included in perioperative fluids, and blood sugars should be monitored frequently intraoperatively and postoperatively.
-patients who undergo bilateral adrenalectomy [some with unilateral surgery as well] will need steroid[Hydrocortisone + Fludrocaortisone] replacement.

If catecholamines are normal, the patient may be one of about 25% of pheochromocytoma patients whose hypertension persists after surgical excision caused by other concomitant disease, such as essential or renal hypertension.

Thanks to Dr Anuj Clerk for contributing this wonderful article.

Compare and contrast persistent vegetative state, locked-in state & akinetic mutism

Persistent vegetative state
* Loss of cognitive neurological function but retains non cognitive functions- respiration,BP, cardiac function etc.
* Lack of consistency in neuro examination; eg.pt may blink, respiration may quicken to stimulation, lack of constant visual following of objects
* EEG- minimal/no change in EEG activity during & after stimulating the patient(i.e no desynchronization)
* Lesion- diffuse cerebral injury, thalamic injury(medial and ventromedian nuclei) & caudal midbrain lesions

Locked-in state
* De-efferented state- patient is alert & aware of environment + quadriplegia+ lower cranial nerve palsy. The only way the patient responds is by vertical gaze & blinking.
* Lesion- involves motor pathways- CS tract, corticobulbar & cortico pontine pathways with sparing of somatosensory pathways & ARAS. The most common site is the ventral pons

Akinetic mutism
* It is a state of altered behaviour where alert appearing patients are silent, inert & profoundly apathetic. They lack psychiatric drive or impulse to action & are doubly incontinent. They usually lie with eyes opened and retain cycles of self-sustained arousal
* Lesion- B/L anterior frontal lobe- this leaves intact motor & sensory pathways

Thanks to Dr Ishaq M for contributing this wonderful article.

Management of Acute Variceal Bleeding

* Gastroesophageal variceal bleeding accounts for 10-30% of upper gastrointestinal haemorrhage and is a major cause of death in patients with cirrhosis.
* The prevalence of oesophageal varices in patients with cirrhosis varies from 24-81%.
* At the time of diagnosis of cirrhosis, oesophageal varices are present in about 60% of decompensated and 30% of compensated patients.
* Despite the high occurrence of varices in cirrhotic patients, only 30% of patients with varices will experience variceal haemorrhage.
* The risk of bleeding appears to be greatest within the first year after diagnosis.
* Mortality of the first bleeding episode is high and ranges between 30% and 50% within 6 weeks; mortality from uncontrolled bleeding in the first instance is between 5-8%.
* Risk factors for the 1st episode of variceal bleeding in cirrhotic patients include - the severity of the liver dysfunction,
- the size of the varices (large greater than small), and
- the presence of endoscopic red wale signs.
- the hepatic venous pressure gradient (HVPG).
* Gastric varices account for approximately 20-30% of cases of variceal bleeding. The prevalence of gastric varices in patients with portal hypertension varies from 6-78% and approximately 25% of gastric varices bleed during lifetime.


General management of bleeding
Patients are usually managed in a high-dependency or intensive therapy unit with facilities for central venous pressure and arterial monitoring.
Therapy is aimed at - correcting hypovolumic shock and resuscitation
- achieving haemostasis at the bleeding site.

This include ABC & resuscitation, initially with plasma expanders and subsequently with blood. If coagulation is defective, replace coagulation factors with fresh frozen plasma. Platelet transfusions may also be required for thrombocytopenia.


Local Haemostasis
An emergency endoscopy should be performed to confirm that varices are the source of bleeding, since peptic ulcer disease is also common in cirrhosis. If possible, endoscopic treatment of varices should be undertaken by endoscopic variceal ligation (banding). Where banding is not possible, sclerotherapy may be useful, adverse events such as oesophageal ulceration and stricture were significantly more severe with sclerotherapy. The most commonly used sclerosants are sodium tetradecyl sulphate (thrombovar) and ethanolamine oleate.


Pharmacotherapy
Octreotide: Decrease portal pressure, 50 micrograms IV, immediately, then 25 to 50 micrograms per hour by IV infusion for 5 days.
While control of initial bleeding has been demonstrated with octreotide, no effect on mortality has been shown. Its transient effect is due to tachyphylaxis.
Terlipressin: 2 mg IV, 6-hourly for 2 to 3 days. It reduces splanchnic blood flow and portal pressure. A meta-analysis demonstrated that terlipressin was associated with a 34% relative risk reduction in mortality compared to placebo.
If endoscopic treatment fails/unavailable and bleeding persists despite octreotide or terlipressin, blood loss can usually be controlled with a Sengstaken-Blakemore–type tube for 24 hours. Balloon tamponade is known to have a high re-bleeding rate when the balloon is decompressed and is associated with serious complications such as ulceration, perforation and aspiration pneumonia. Thus, this should only be considered if facilities for endoscopy are not available prior to transfer to a tertiary centre or as a temporary ‘bridge’ for a maximum of 24 hours until definitive treatment can be instituted.

Antibiotics in Acute Variceal Bleeding
Bacterial infections are seen in about 20% of cirrhotics presenting with upper gastrointestinal bleeding within 48 hours. The incidence of sepsis increases to almost 66% at two weeks. Development of bacterial infection is associated with high mortality and variceal re-bleeding. Antibiotic prophylaxis has been shown to reduce the rate of infection, spontaneous bacterial peritonitis and rebleeding. In addition, antibiotic prophylaxis was clearly proven in a meta-analysis to significantly increase the survival rate. Short-term antibiotic prophylaxis for 7 days should be considered the standard of care in cirrhotic patients with upper gastrointestinal bleeding, irrespective of the type of haemorrhage (variceal or nonvariceal) or the presence or absence of ascites. As to the choice of antibiotic, either third generation cephalosporins given intravenously or oral quinolones (norfloxacin/ciprofloxacin) are generally recommended.

Continued bleeding
Continued bleeding is associated with a high mortality. A second course of endoscopic treatment may be undertaken with continued use of a Sengstaken-Blakemore–type tube for up to 24 hours. Adjunctive infusion of octreotide can be given. An emergency transjugular intrahepatic portosystemic shunt (TIPS) or an emergency portosystemic shunt may be considered, depending on available local expertise.
Transjugular intrahepatic portosystemic shunts (TIPS) is effective in the treatment of acute variceal bleeding with a success rate of over 90% in arresting haemorrhage. The main limiting factors to the use of TIPS are the high morbidity and mortality: the 30-day mortality approaches 100% in patients with advanced liver disease, ongoing sepsis and multi-organ failure. Therefore, the most widely accepted indication for TIPS is as a rescue therapy for uncontrolled variceal bleeding after combined pharmacological and endoscopic therapy.

Surgical Therapy
Surgical options include oesophageal transection with or without devascularisation, portosystemic shunts and liver transplantation. Regardless of the choice of the surgical technique, morbidity and mortality are high: the 30-day mortality associated with emergency surgical procedures is nearly 80%. Similar to TIPS, the role of surgical therapy in the management of acute variceal bleed has been relegated to salvage haemostatic therapy. Liver transplantation is probably only appropriate for liver transplant candidates who bleed while on the waiting list.

Prevention of rebleeding
In patients with cirrhosis who have bled from oesophageal varices, the risk of rebleeding within 12 months is about 60%. Measures to reduce this risk include regular endoscopic banding until varices have largely disappeared. In the longer term, varices recur and may need further banding. In a meta-analysis of clinical trials, therapy with propranolol has been shown to reduce recurrent variceal bleeding and improve survival. In those who rebleed despite the above therapy, TIPS, portosystemic shunt or transplantation should be considered.