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.

Takotsubo Cardiomyopathy

Recently came across two cases of Takotsubo syndrome. One of them diagnosed during angiography (normal with typical apical balloning. Here is synopsis of this cardiomyopathy, further reading can be done from various resources, however, one good site is http://www.takotsubo.com/

Essentials of Diagnosis
Occurs after a major catecholamine discharge.
Acute chest pain or shortness of breath.
Predominately affects postmenopausal women.
Presents as an acute anterior myocardial infarction, but coronaries normal at cardiac catheterization.
Imaging reveals apical left ventricular ballooning due to anteroapical stunning of the myocardium.

General Considerations
LV apical ballooning can follow a high catecholamine stress. The resulting shape of the LV suggests a rounded ampulla form similar to an octopus pot (takotsubo pot). The acute myocardial injury that occurs is more common in postmenopausal women. It has been described following some stressful event, such as hypoglycemia, lightning strikes, earthquakes, postventricular tachycardia, during alcohol withdrawal, following surgery, during hyperthyroidism, and following emotional stress.

Clinical Findings
Symptoms and Signs
The symptoms are similar to any acute coronary syndrome. Typical angina and dyspnea is usually present. Syncope is rare.

ECG and Chest Radiography
The ECG reveals ST segment elevation as well as deep anterior T wave inversion. The chest radiograph is either normal or reveals pulmonary congestion.

Diagnostic Studies
The echocardiogram reveals LV apical dyskinesia. The urgent cardiac catheterization reveals the LV apical ballooning in association with normal coronaries.



TreatmentImmediate therapy is similar to any acute myocardial infarction. Initiation of long-term therapy depends on whether LV dysfunction persists. Most patients receive aspirin, -blockers, and ACE-inhibitors until the LV fully recovers.

Prognosis
Prognosis is good unless there is a serious complication (such as mitral regurgitation, ventricular rupture, ventricular tachycardia). Recovery is expected in most cases after a period of weeks to months. At times, the LV function recovers in days.

Horners syndrome in ICU

 Components
 Reason/relevant clinical anatomy
 Etiology
 Diagnosis

Components- Ptosis, miosis, anhydrosis(classic triad), enophthalmus, chemosis of conjunctiva, nasal stuffiness.

Reason- lesion anywhere in the sympathetic neural pathway supplying the head and neck(oculo sympathetic defect)
Relevant clinical anatomy- ocular sympathetics is a 3 neuron ipsilateral pathway:
1st order neurons- arise from hypothalamus and synapse with
2nd order neurons- pre-ganglionic fibres located in the intermediolateral spinal cord, C8-T2 (cilio spinal centre of Budge)- they exit in the anterior roots and pass over the pulmonary apex to synapse in the superior cervical ganglia (located near the angle of jaw).
3rd order neurons- Post ganglionic fibres- run along with the internal carotid artery as sympathetic plexus surrounding it & enter the skull. They exit the skull via orbit in the ophthalmic division of trigemminal nerve and supply the following- Mullers muscle (levator palpebrae superioris) of the upper eyelid, radial muscle of iris (dilator pupilae) and sweat gland of face.


- Horner's syndrome + brain stem/cerebellar signs => suspect a brain stem or cerebellar stroke syndrome affecting the first neuron eg. Wallenberg' syndrome
(* a "central" Horner's syndrome affecting the first neuron does not respond to cocaine and the diagnosis must be made by the associated neurological signs - nearly always associated with pain and temperature loss on the opposite side of the body)

- Horner's syndrome + sensory and/or motor deficit of the limbs => suspect cervical spinal cord pathology affecting the first neuron

- Horner's syndrome + hoarseness => compressive lesion in the chest or neck affecting the second neuron and recurrent laryngeal nerve

- Horner's syndrome + paralysis of the ipsilateral phrenic, vagus and recurrent layngeal nerve => tumor behind the carotid sheath at the C6 level affecting the second neuron

All patients with an unexplained unilateral Horner's syndrome + face/head pain should be presumed to have a carotid artery dissection until proved otherwise

- the sympathetic nerves to the eye travel with the ophthalmic nerve (V1) and a lesion affecting V1 in the region of the orbit is also likely to affect to neighbouring nerves

- Horner's syndrome + cranial nerve 3 and/or 4 and/or 6 and/or V1/V2 dysfunction (and not affecting V3) => suspect cavernous sinus pathology

- Horner's syndrome + cranial nerves 3 and/or 4 and/or 6 and/or V1 (and not affecting V2 and V3) dysfunction => suspect superior orbital fissure pathology

- Horner's syndrome + cranial nerves 2 (optic nerve), 3, and/or 4 and/or 6 and V1 (and not affecting V2 and V3) dysfunction => suspect orbital apex pathology

- Horner's syndrome + optic nerve II dysfunction +/- incomplete cranial nerve 3 dysfunction (and not affecting cranial nerves 3, 4 and 6 and V2 and V3) => suspect posterior orbit pathology

- all patients with an asymptomatic, unexplained Horner's syndrome (especially if they have ipsilateral anhidrosis of the face and neck, which implies a preganglionic Horner's syndrome), who are going to be discharged from the ED for pre-arranged follow-up as an outpatient, should have a chest X-ray performed prior to ED discharge - to exclude a mediastinal or apical lung tumor (Pancoast's tumor) or thoracic aneurysm affecting the second neuron


Etiology-
In general- brain stem lesions (stroke, tumour, trauma), cervical cord lesions, pancoast syndrome & iatrogenic
In ICU- iatrogenic causes are more important (10% of all cases of horners syndrome admitted to hospital)- neck surgery, carotid angiography/endartrectomy/surgeries(are well recognized causes), IJV cannulation and ICC placement. Other causes are- brachial plexus block and thoracic epidural anesthesia. The close proximity of cervical sympathetic trunk to the IJV may result in damage to the trunk by either trauma from the needle or pressure from a hematoma with he development of Horners syndrome. The risk of damaging the sympathetic fibres is increased with a higher approach to the IJV and if the angle between the needle and the skin is great. In the ICU patients with sudden onset of U/L miosis, the d/d is between carotid dissection vs. horners syndrome; the relevant clinical context becomes important to
differentiate.

Clinical Tests for diagnosis-
Dilation lag of miotic pupil- where in dark, the miotic pupil initially fails to dilate increasing the degree of anisocoria- considered specfic test
Cocaine test- Gold std- failure of cocaine drops to dilate the miotic pupil

Differentiation between physiological anisocoria and Horner's syndrome

Accidental hypothermia – Clinical Effects

Accidental hypothermia is defined as an unintentional decline in core temperature below 35°C (95°F).

•Primary hypothermia occurs because of accidental exposure to cold.
The difference between ambient and core temperature does not have to be great. Since most heat generation occurs through muscle activity, as long as the level of muscle activity required to keep up with heat loss is sustained, the core temperature is maintained. As the ambient temperature remains low, fatigue eventually occurs and muscle activity declines or ceases, and the core temperature falls. Physical conditioning, dehydration, and lack of caloric intake necessary to feed the required muscle activity are examples of factors that exacerbate the problem (this often occurs in recreational situations by accident, misfortune, or stupidity). Medical conditions such as strokes or other injuries may prevent muscle activity or behavioral responses to cold, causing or worsening hypothermia.

•Secondary hypothermia occurs when a disease state causes failure of thermoregulatory function. A high index of suspicion is necessary to accurately diagnose and treat secondary hypothermia since many causes are possible, and treatment is predicated on identification and correction of the underlying abnormality.

At temperatures < 35°C (95°F), the patient becomes less capable of generating heat, and body temperature continues to fall unless some action is taken.
At a core temperature < 30°C (86°F), the body assumes the temperature of the surrounding environment.

Heat is lost or gained through several physical mechanisms, including radiation, conduction, convections, and evaporation. Radiation may account for 55% of loss, evaporation 30%, and conduction 15%, with convection being a relatively minor component. Being wet or immersed in water causes more rapid heat loss.

Air < water (25 X) < ground < Concrete/stone ( 100 X)

A physiologic heat balance is a result of many variables, including the ability to generate heat, body size, age, insulation in the form of clothing, and the temperature of the environment to which the patient is exposed. Heat always flows from a warmer object to a colder object. Under most circumstances the body is warmer than the surrounding environment; thus, the natural flow of heat is out of the body.

3 mechanisms contributing(alone or together) to hypothermia
Reduction in heat production
Endocrine disorders
Myxoedema, Addison’s disease, hypopituitarism, diabetic ketoacidosis, hypoglycaemia, lactic acidosis
Severe infection
Septicaemia, pneumonia, peritonitis, pyelonephritis, meningitis
Malnutrition
Wernicke’s encephalopathy
Uraemia
Cirrhosis
Pancreatitis

Increased heat loss
Cardiovascular accident
Major surgery
Burns, exfoliative dermatitis
Trauma
Massive transfusion
Renal replacement therapy, dialysis
Drugs : ethanol, opiates, barbiturates, benzodiazepines, phenothiazines, tricyclics

Loss of Thermoregulation

Clinical
History
Because hypothermia may accompany a more obvious condition, considering hypothermia in the differential diagnosis in any patient is critical, especially those who present with unexplained symptoms. Remembering that symptoms of a primary condition, such as a stroke, may overshadow the symptoms of hypothermia is also important.
•Symptoms are vague
•Clinical manifestations
•Risk factors include recreational exposure to a cold environment
•Trauma
•Drug use or an overdose
•Inadequate clothing for ambient temperatures
•Hypothermia as a complication of underlying diseases

Physical
Mild hypothermia (32-35°C or 89.6-95°F) : In normal individuals shivering usually occurs when the core temperature is reduced by 0.7°C (increasing the metabolic rate by up to 5 times). When the temperature is reduced to 35°C the patient usually shivers uncontrollably. The reduction in temperature also produces dermal vasoconstriction, tachycardia, elevation of the cardiac output, elevation of plasma catecholamine levels, a ‘cold’ diuresis and hyper-glycaemia. If glycogen stores are depleted, hypo-glycaemia may occur which inhibits shivering. The plasma levels of thyrotropin releasing hormone (TRH), triiodothyronine (T3), L-thyroxine (T4), growth hormone, thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH) stimulation tests are normal, suggesting normal pituitary, adrenal and thyroid function during mild hypothermia. other features are Ataxia, Dysarthria, Loss of fine motor coordination, Lethargy, apathy, confusion, impaired judgment

Moderate hypothermia (28-32°C or 82.4-89.6°F) : At temperatures below 33°C, shivering gradually decreases, muscle and joints become stiff and there is a delayed relaxation phase of the stretch reflexes. The patient becomes lethargic, drowsy and often falls asleep. Unconsciousness rarely occurs at temperatures above 28°C, so another cause of coma should be sought if coma exists at levels above this temperature. The pulse, blood pressure and respiratory rate are usually depressed. J waves on ECG and Cold diuresis.





Severe hypothermia (<28°C or 82.4°F) : At a temperature below 30°C, the body loses its ability to spontaneously return to a normal temperature (i.e. the patient becomes poikilothermic); thus active rewarming must be performed. At a temperature below 28°C, the patient is unconscious, areflexic with fixed and dilated pupils, and life may be difficult to detect. Bradycardia and atrial fibrillation occur at temperatures below 30°C and ventricular fibrillation (VF) may occur at temperatures below 28°C. At 20°C asystole is more common than VF. Respiratory frequency maybe reduced to 1 - 2 breaths/min. Bronchorrhoea is common (probably due to deficient ciliary function), whereas pulmonary oedema is rare. Circulatory arrests for 10 min at 30°C, 25 min at 25°C, 45 min at 20°C and 60 min at 16°C are often quoted as being the limits at which cerebral function may return to normal, although case studies indicate that these limits can be extended.The lowest temperature recorded in a person who has subsequently survived is 16.4°C, although under controlled hypothermic conditions for surgical procedures, temperatures down to 10°C are used, and temperatures as low as 6°C have been recorded.

Onset of hypothermia can be triggered by events similar to the generation of primary hypothermia, and primary and secondary hypothermia may exist concurrently. For example, when a patient has a stroke (disruption of thermoregulation due to CNS injury) and falls to a concrete floor (heat loss through conduction) and cannot get up (failure of behavioral adaptations to cold), hypothermia may ensue.