2018 SAQ in ICM

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 4  Measures may reduce the Risk of development of VAP VAP bundle: General measures: Use of sterile equipment, regular hand washing, u

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Short Answer Questions

Anaesthesia

& Intensive Care

Part: 1 - Intensive Care Medicine

Modified by

AYMAN EDAROUS

Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]

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MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 2

For Original Materials and Editors, Please refer to:

North Ireland School of Anaesthesia Website

http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/intensivecare/

ميحرلا نمحرلا هللا مسب

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1- Ventilator Associated Pneumonia (VAP)

a) What is meant by the term Ventilator Associated Pneumonia (VAP)? (3 marks)

b) List the factors that increase the risk of the development of VAP (10 marks)

c) What measures may reduce the risk of development of VAP? (7 marks)

 Ventilator Associated Pneumonia (VAP):

Pneumonia occurring 48-72 hours after ETT intubation,

characterised by (Diagnostic Criteria):

-Clinical Signs: Pyrexia, raised WCC, Purulent Bronchial Secretion

-Microbiological Evidence: Positive Sputum Culture

-Radiological Signs: New or Progressive Pulmonary Infiltrates

The common pathogens associated with VAP:

Mainly caused by G-ve organisms, but G+ve bacteria such as MRSA are not uncommon

Typically, bacteria causing early onset VAP include:

Culprits of late VAP are drug-resistant organisms such as MRSA, Acinetobacter, Pseudomonas

aeruginosa, and extended-spectrum beta-lactamase producing bacteria (ESBL)

Pathogenesis of VAP:

 It is thought to be caused by entry of infected secretions into distal bronchi

 Patients are usually immunosuppressed, and their oropharynx becomes colonised with organisms, especially G-ve bacteria

 Oral and nasal tubes cause trauma, leading to infections such as sinusitis

 The natural protections like cough reﬂex, tracheobronchial secretions, mucociliary linings, saliva, and nasal mucosa are less effective in these patients

 The pathogens enter the lower lung through mechanical routes such as around the

endotracheal tube cuff, suction catheter, and ventilation tubings

 Factors that Increase the Risk of the Development of VAP:

1- Patient factors 2- Interventional factors:

Advanced age

Low serum albumin

ARDS, COPD and other lung diseases

Impaired consciousness

Trauma and Burns

Multiple Organ Failure

Large volume gastric aspirates

Upper respiratory tract colonisation

Frequent circuit changes

Transfer outside ICU

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 Measures may reduce the Risk of development of VAP (VAP bundle):

General measures: Use of sterile equipment, regular hand washing, using barrier nursing such as gloves and an apron, and minimal contact with patient usually reduce the incidence of any infection

in ICU

Specific measures: This include reducing the load of pathogens and their entry into lower

respiratory tract

Reducing Oral Colonisation

*Good Oral Cavity Care including Regular Brushing of Teeth

*Use of Antiseptic Mouthwash (e.g Chlorhexidine)

*Use of Silver coated ETT (prevents build up of Biofilms on ETT lumen)

*Selective decontamination of digestive tract (SDD) using non-absorbable

antimicrobials such as Polymyxin E and Amphotericin B has been tried with

variable success [NB: It encouraging Clostridium diffcilie, antimicrobial

resistance, and the emergence of multi-drug resistant pathogens]

• Reducing Aspiration

*Patients nursed in 30-45o degree head-up position

*Use of ETT with subglottic secretion drainage port with regular subglottic suction

*Regular Monitoring /4 hr and maintainence of ETT Cuff Pressure (20-30 cmH2O)

• Minimising duration of Mechanical Ventilation:

*This is achieved by early tracheostomy, which has proven to lower the incidence of VAP

*Periodic ‘sedative interruptions’ and daily assessment of readiness to extubate may reduce the duration of mechanical ventilation

• Stress Ulcer Prophylaxis:

*Reducing the acidity of stomach in stress ulcer prophylaxis

is claimed to increase the incidence of VAP by increasing

the proliferation of gram-negative bacteria Use of H2

blockers or Sucralfate, instead of PPIs, are suggested to

reduce the risk

*Enteral feeding can increase the risk of VAP by altering the

gastric acidity and risk of aspiration, but benefits of enteral

feeding usually outweigh this small risk

•Deep Venous Thrombosis (DVT) Prophylaxis:

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Clinical Pulmonary Infection Score (CPIS) for VAP

The CPIS takes into account:

 Clinical:Temperature, Presence of tracheal secretions

 Physiological: Leucocytosis and worsening gas exchange

 Microbiological: Positive culture of tracheal aspirate

 Radiographic: evidence to assign a numerical value

**Scores can range from 0 to 12 with a score of ≥ 6: good correlation with the presence of VAP

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2- Surviving Sepsis Campaign 2018

You are asked to assess a 45 year old woman in A&E resus who has a provisional

diagnosis of Gallbladder Sepsis

a) Define (i) Sepsis (ii) Septic Shock (25%)

b) What diagnostic criteria for sepsis as suggested by the 2012 Surviving Sepsis Campaign would you apply to this patient? (25%)

c) Outline the targets for management and categorise into accepted timeframes (25%)

d) What are the major changes in the 2012 recommendations compared to the original? (25%)

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 Diagnostic criteria for sepsis as suggested by the 2016 Surviving Sepsis Campaign:

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 The Targets for Management:

Hour-1 Surviving Sepsis Campaign Bundle of Care (2018)

Te most important change in the revision of the SSC bundles is that the 3-h and 6-h bundles have been

combined into a single “hour-1 bundle” with the explicit intention of beginning resuscitation and

management immediately We believe this reflects the clinical reality at the bedside of these seriously ill patients with sepsis and septic shock-that clinicians begin treatment immediately, especially in patients with hypotension, rather than waiting or extending resuscitation measures over a longer period

More than 1 h may be required for resuscitation to be completed, but initiation of resuscitation and treatment, such as obtaining blood for measuring lactate and blood cultures, administration of fluids and antibiotics, and in the case of life-threatening hypotension, initiation of vasopressor therapy, are all begun immediately

 Measure Lactate Level

If initial lactate is elevated (> 2 mmol/L), it should be re-measured within 2–4 h to guide resuscitation

to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion

 Obtain Blood Cultures (prior to Antibiotics)

Sterilization of cultures can occur within minutes of the first dose of an appropriate antimicrobial, so cultures must be obtained before antibiotic administration to optimize the identification of pathogens and improve outcomes Appropriate blood cultures include at least two sets (aerobic and anaerobic) Administration of appropriate antibiotic therapy should not be delayed in order to obtain blood

cultures

 Administer Broad-Spectrum Antibiotics

Empiric broad-spectrum therapy with one or more intravenous antimicrobials to cover all likely

pathogens should be started immediately for patients presenting with sepsis or septic shock Empiric antimicrobial therapy should be narrowed once pathogen identification and sensitivities are

established, or discontinued if a decision is made that the patient does not have infection The link between early administration of antibiotics for suspected infection and antibiotic stewardship remains

an essential aspect of high-quality sepsis management If infection is subsequently proven not to exist, then antimicrobials should be discontinued

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 Administer Intravenous Fluid

Initial fluid resuscitation should begin immediately

upon recognizing a patient with sepsis and/or

hypotension and elevated lactate, and completed

within 3 h of recognition The guidelines

recommend this should comprise a minimum of 30

ml/kg of intravenous crystalloid fluid

Because some evidence indicates that a sustained

positive fluid balance during ICU stay is harmful,

fluid administration beyond initial resuscitation

requires careful assessment of the likelihood that

the patient remains fluid responsive

 Apply Vasopressors

If blood pressure is not restored after initial

fluid resuscitation, then vasopressors should

be commenced within the first hour to

achieve mean arterial pressure (MAP) of ≥ 65

mmHg

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MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 11 The major changes in the 2016 recommendations compared to 2012:

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PATHOPHYSIOLOGY

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3- Acute Respiratory Distress Syndrome (ARDS)

(a) What are the defining features of ARDS (according to the 2012 ARDS Definition Taskforce)?

(b) Why was a new definition felt to be necessary?

(c) Describe the pathophysiology of ARDS

(d) Describe the management of ARDS in the ICU

 Berlin Definition of ARDS:

 Why was a new definition felt to be necessary?

A number of issues regarding the old definition had emerged Including:

*No explicit criteria for defining Acute

*High inter-observer variability in interpreting chest X-rays

*Difficulties in ruling out cardiogenic causes of pulmonary oedema

*PaO2/FiO2 ratio is sensitive to changes in ventilatory settings

*Intensive care societies felt a definition that simplified the diagnosis and better prognosticated

outcomes was needed

*The new definition predicted Mortality ever so slightly better than the existing definition however the power of the new definition to predict mortality is still poor with an area under the curve of only 0.577 vs 0.536 for the old definition

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 The Pathophysiology of ARDS:

Regardless of the cause disease progression is the same

Acute Phase:

*Lasts for up to 7 days from Onset

*Hypoxemia, Infiltrates on the Chest Radiograph, and  in Pulmonary Compliance

*Leakage of Protein-rich fluid into the Alveoli, Haemorrhage, and Diffuse Neutrophilic Alveolar

Infiltrate with resultant Endothelial and Epithelial Injury

Proliferative Phase:

*Can occur from day 5 onwards

*Characterised by persistent Hypoxaemia,  Dead Space, and  Lung Compliance

*Accompanied by Interstitial Fibrosis, Proliferation of type 2 Alveolar Cells, and disruption of Capillary function due to Microvascular Thrombus Formation

*In some these changes resolve and clinical improvement follows; others progress into the Chronic or Fibrotic Stage

Chronic Phase (Fibrotic Stage):

*Not clearly defined

*May starts as early as day 14 and can Last Weeks

*Widespread Pulmonary Fibrosis and Loss of the normal Lung Structure leads to worsening Lung Compliance and an  in Dead Space

*Clinically there is a  in CO2 excretion which may be accompanied by an improvement in

Protective Lung Ventilation:

-Aim of mechanical ventilation is to maintain

adequate gas exchange until cellular damage

resolves without causing ventilator induced lung

injury

*ARDSnet Tidal Volume study showed:

-High volume ventilation damages remaining healthy

lungs

-Low volume ventilation had significantly lower level of

circulatory cytokines, biotrauma and distant end organ

damage

-PEEP improved Oxygenation by maintaining patency

of injured alveoli, improvement in V/Q mismatch, 

in Shunt and preventing Atelectrauma

Study couldn’t show superiority of high over low PEEP

-Conclusion: Vt of 6ml/kg, Peak Pressures of less than 30cmH2O and PEEP

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Activated neutrophils adhere to endothelial cells and release inflammatory mediators, including oxygen-free radicals and proteases, to cause lung damage Direct lung damage or endotoxins alone are sufficient to damage endothelial cells with cytokine release and an inflammatory cascade Endothelial damage results in increased capillary permeability and formation of protein-rich alveolar exudate rich in neutrophils Type I alveolar cell are damaged and type II cells proliferate As the disease progresses, fibroblast infiltration and collagen proliferation cause microvascular obliteration

and widespread fibrosis Areas of lung involvement are not fixed but shift to dependent areas Within areas of reduced lung volume, some alveoli remain open and capable of gas exchange, whereas others are filled with alveolar exudate IPPV may cause damage more through excess volume (‘volutrauma’) than through pressure itself The significance of oxygen toxicity is controversial

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Circulatory support and Fluid Management:

FACTT trial showed conservative fluid management had a reduced number of days ventilated and reduced ICU stay Reductions in lung water with diuretics +/ albumin

Treatment of the Cause: Antibiotic for Pneumonia

Glycaemic Control.

DVT Prophylaxis

Gastric Ulcer Prophylaxis.

Ventilator bundle

 Central Catheter Care Bundle

Early Enteral Feeding.

 Other Interventions of improving Oxygenation:

-Nitric Oxide

-Steroids:  edema.

-Activated protein C

-Intravenous B-agoinst therapy

-Prone Position enhances oxygenation and improves V/Q mismatching but at the minute hasn’t been shown to improve survival overall

-Other trials are ongoing, eg Statins for their ability to decrease inflammation

-High frequency oscillatory ventilation (HFOV)

- ECMO: used to rescue some patients with severe ARDS who have primary single organ failure

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4- Severe Acute Pancreatitis

(a) Briefly describe the anatomy of the pancreas

(b) What are the signs and symptoms of acute pancreatitis?

(c) How may it be further diagnosed?

(d) Describe a method of prognostication in the disease

(e) What are the potential short and long term complications of pancreatitis?

 Anatomy of The Pancreas:

- Retroperitoneal organ, located at T12.

- Head lies centrally

-Tail extends to overlap part of left kidney

- Connects to duodenum via ampulla of vater

- Arterial: branches of SMA, splenic A

- Venous: SMA, splenic, portal

- Nervous: coeliac, superior mesenteric plexus

- Has functional Endocrine and Exocrine units

(Islets of Langerhans, Acini)

 Causes of Pancreatitis (I GET SMACHED):

Signs and Symptoms:

History:

- Risk Factors e.g alcohol excess, gallstones, drugs,

previous incidents

- Severe upper abdominal pain radiating to back,

relieved by sitting forward

- Nausea and vomiting

Examination;

- Systemically unwell; SIRS response

- Abdominal distension, peritonism,

-Grey Turners (flanks)

-Cullens (peri umbilical) discoloration secondary to

retroperitoneal hge

- Evidence of end organ dysfunction e.g Respiratory Distress, Oligouria, Jaundice

 Further Diagnosis:

- Serum Amylase (> 3X), Lipase (> 3X), Tryptase

- CT scan early if diagnosis uncertain, at 48-72

hours for Prognostication and Management

-MRCP, Endoscopic ultrasound (EUS) and USS

(diagnosis of gallstones)

 Complications of Pancreatitis:

Patients with severe pancreatitis can have systemic

and local complications, including:

Pleural effusion, ARDS, ileus, Gastric ulceration,

Renal failure and cardiovascular compromise

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Local complications include acute fluid collection leading to gastric outlet obstruction, pseudocyst, Abscess, Necrosis, Pseudoaneurysm of the splenic artery and fistulation into an adjacent hollow viscus

 Prognostic Methods:

*APACHE II score: [Physiological Parameters and a Chronic Health Evaluation]

Score greater than 8 predicts a severe episode of pancreatitis,

maximum score 71

*Modified Imrie/Glasgow score

-Described features in a population of patients with gallstone

pancreatitis

-Score greater than or equal 3 predicts a severe episode of

pancreatitis

*Ranson's Score:

Developed from an American of alcohol induced pancreatitis

*Balthazar CT Severity Index

*BISAP score

 Management:

Early identification and management of

organ failure and aggressive resuscitation to

optimise tissue perfusion is important in

cases of severe pancreatitis

Cholecystectomy in cases of mild

gallstone-induced pancreatitis should be performed

within 2 weeks of discharge In cases of

severe pancreatitis, surgery should be

performed

once the patient has recovered

- Pancreatic Necrosis

- Peripancreatic fluid collection;

sterile and infected

- Massive Haemorraghe

- Haemorragic Pancreatitis

- Portal Hypertension

- Procoagulant state with VTE

- Abdominal Compartmental Syndrome

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5- Acute Kidney Injury (AKI) and Dialysis

(a) What is Acute Kidney Injury (AKI)? How might it be classified? (20%)

(b) What investigations should be performed in a patient in acute renal failure? (20%)

(c) What is your management of a patient admitted with ARF to ICU? (20%)

(d) Describe a RRT circuit - how does it work to remove fluid and solutes? (20%)

(e) What are the different methods of anticoagulation in patients on RRT? (20%)

 Acute Kidney Injury (AKI):

An abrupt (within 48 hours) Reduction in Kidney Function, defined as:

An absolute increase in serum Creatinine of at least 0.3mg/dl (26.4micromol/L),

OR

A percentage increase in serum creatinine of at least 50% (1.5x baseline)

OR

A reduction in urine output to 0.5ml/kg/hour or less for over 6 hours

- Acute Kidney Injury Network (AKIN) 2007 Modified RIFLE Classification:

 The Investigations should be performed in a patient in Acute Renal Failure:

Kinase(CK)/urinary Myoglobin, Urinary Sodium, Urine plasma:osmolality ratio, Urine Microscopy, U/S renal tracts

-Rate at which Substances are Filtered from the Blood of the Glomeruli into the Bowman’s

Capsules of the Nephrons

-Calculated by the clearance of specific substances which have a constant plasma concentration, are freely filtered by the glomerulus, and are not subsequently secreted, reabsorbed or

metabolised The clearance of substances from the plasma are used as an index of GFR

-Creatinine clearance is the most common in clinical use

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differentiate between Prerenal and Intrarenal disease

 Management of a patient admitted with ARF to ICU:

Avoid hypoxaemia, ventilate if necessary

adequate fluid loading has been achieved, Inotropic and Vasopressor support can be used to achieve

an appropriate MAP

Hold Nephrotoxins (e.g NSAIDs, ACE-Is, Contrast Media)

-Severe Metabolic Acidosis related to tubular dysfunction can be corrected with sodium bicarbonate

-Supportive: diuretic therapy, renal replacement therapy

-Definitive: surgical decompression

Removal of offending agent (penicillin, cephalosporins)

*Hyperkalaemia: (s K+ > 6.5 mmol/L with ECG abnormalities)

*Uraemia: (>35mmol/L): Encephalopathy, Pericarditis, Bleeding

*Acidaemia: (pH<7.1) ,

*Fluid Overload : resistant to diuretics

 RRT circuit and how does it work to remove fluid and solutes:

Intermittent RRT:less expensive, simpler to run, requires less time, rapid fluid and solute removal is possible However, critically unwell patients may become haemodynamically unstable, and

hypotension may cause further renal injury

Continuous RRT: slower and more expensive than Intermittent, and requires premixed fluids and anticoagulation Slower fluid and solute removal reduces risk of haemodynamic instability

Peritoneal: inefficient at removing large amounts of fluid/solute Increases intra-abdominal pressure, which may splint diaphragm in unwell patients, so contraindicated in critical care

-Veno-Venous circuit -pump driven, reliable high flow rates Commonly used now

-Arterio-Venous circuit –driven by patients own BP Less reliable, associated with catheter related complications, so rarely used now

Mechanism of Fluid Removal ( Ultrafiltration ):

Produced by creating a positive pressure in the blood compartment of the dialyser and is facilitated

by creating a negative pressure in the dialysate compartment The resulting trans-membrane

pressure is the driving force for ultrafiltration

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Mechanisms of Solute Removal ( Haemodialysis )

Diffusion (Principle Process during Haemodialysis): The spontaneous migration of substances from regions where their concentrations are high to regions where their concentrations are lower During haemodialysis, diffusive transport is driven by the solute concentration gradients that exist between blood and dialysate The dialysate runs countercurrent to blood flow, separated by a semipermeable membrane

Convection/ Hemofiltration (Solvent Drag): Occurs when a solute molecule is swept through a

membrane by a moving stream of ultrafiltrate Convective transport is independent of any solute concentration gradients that may be present across a membrane The porosity of the membrane is a major determinant of which molecules are removed but only the direction and force of trans-

membrane fluid flux determine the amount of convective transport

 The Different Methods of Anticoagulation in Patients on RRT:

-Exposure of blood to a non-biological surface (the filter membrane) activates the clotting cascade -Aims of anticoagulation are to prolong filter life (prevent “clotting off”), whilst minimising systemic anticoagulation

-Typically a bolus followed by a prefilter infusion

-Cost effective, can be fully reversed with protamine

-Requires monitoring of APTT

Low Molecular Weight Heparin:

-Lower incidence of heparin-induced thrombocytopenia

-Longer half-life than UFH, only partially reversed by protamine

Prostaglandins:

-Inhibit platelet function Can be used alone, or with heparin (synergistic effect)

-Short half-life, so administered as infusion

-Potent vasodilator, so can reduce MAP

-May inhibit hypoxic pulmonary vasoconstriction, so may cause/worsen hypoxaemia

-Expensive

Sodium Citrate:

-Infused prefilter

-Chelates calcium and inhibits clot formation

-Calcium infusion required post filter

-Cause metabolic derangements (hypoCa, hypoMg, hyperNa, metabolic alkalosis, or acidosis)

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Fig For the hemodialysis circuit, the green bag represents the dialysate and the yellow bag the used dialysate For the hemofiltration circuit, the yellow bag represents the ultrafiltrate and the purple

bag the postdilution replacement fluid.

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6- Guillain Barre Syndrome (GBS)

(a) What is Guillain Barre Syndrome (GBS)? How is it sub classified?

(b) What are the symptoms and signs of GBS?

(c) How is it diagnosed?

(d) What is the differential diagnosis?

(e) Describe the airway management in GBS What parameters are used to decide to intubate?

 Guillain Barre Syndrome (GBS):

- An Acute Demyelinating Polyneuropathy

- It is an Auto-immune phenomenon due to GI or Respiratory

Infection (Campylobacter jejuni, EBV, CMV, HIV …) or

Vaccination

- Males are more affected

Several different Clinical Pictures exist:

 Acute Inflammatory Demyelinating Poly-radiculopathy

with prolonged or only partial recovery

*It is unique in that this subtype begins with cranial nerve deficits (III – VII and IX – XII)

*Patients present with facial weakness mimicking Bell’s palsy, dysphagia, dysarthria,

ophthalmoplegia, and pupillary disturbances

has a chronic and relapsing course

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 Symptoms and Signs of GBS:

 It should be suspected in any patient with unexplainable weakness or sensory deficit affecting the limbs Signs and Symptoms vary according to subtype

Motor Dysfunction:

- Progressive Motor Weakness, usually Symmetric, Ascending from the Legs

Sensory Dysfunction:

-Pain is most severe in the shoulder girdle, back, buttocks, and thighs

-Paraesthesia and Numbness usually begins in the toes and fingertips and progresses upward but generally does not extend beyond the wrists or ankles

-Loss of vibration, proprioception, touch, and pain distally may be present

Autonomic Dysfunction:

-Tachycardia, Arrythmia, Labile Blood Pressure, Orthostatic Hypotension

-Urinary Retention, Paralytic Ileus and Hyperhydriasis

 Diagnosis:

- GBS should be suspected in all patients with unexplained motor weakness or a new sensory deficit affecting the limbs

History: of recent Gastrointestinal or Respiratory infection should be sought

Examination: Symptoms and Signs (SEE BEFORE)

Investigations:

- Daily measurement of Vital Capacity

- Lumbar Puncture/ CSF analysis:  Protein and Normal WBC

- Electrophysiological Studies: aid diagnosis and help to differentiate GBS from other

neuropathies Each subtype has different electrophysiological features

- Muscle biopsy: may help to distinguish GBS from a primary myopathy in unclear cases

- MRI: May show spinal nerve root enhancement with gadolinium

- Stool Cultures may show Campylobacter jejuni infection

- Blood Tests: Anti-Ganglioside Antibody Anti-GM1 antibodies are associated with a worse

prognosis and Anti-GQ1 antibody is associated with MFS

 The Differential Diagnosis:

Neurological: Myasthenia gravis, Eaton-Lambert syndrome, MS and transverse myelitis

Metabolic: Hypokalaemia, Hyper-Mg4, Hypophosphataemia and Acute Intermittent Porphyria Infective: Post Diptheria Neuropathy, Polio, Botulism and Tick Paralysis

Drugs/Toxins: Heavy Metal Poisoning (eg Lead), biological Toxins (eg Snake and Scorpion toxins) and drugs (eg Nitrofurantion and Aminoglycosides)

Other: Acute Polymyositis and Intensive Care Unit Acquired Weakness

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 Management of GBS ( ABCD protocol):

Airway

- 30% of patients require ventilatory support

- Deterioration in respiratory function may be rapid and patients should have three times daily measurement of Vital Capacity

Clinical Indictors for Intubation:

 Vital Capacity < 20ml/kg

 Max Inspiratory Pressure (MIP) < -30 cmH2O

 Max Expiratory Pressure (MEP) < 40 cmH2O (the 20/30/40 Rule)

 Bulbar involvement with Inability to Cough or Protect The Airway

 Respiratory Failure on Blood Gas

 Autonomic Instability

Breathing

Patients with the following features are 85% likely to need Mechanically Ventilated

[Predictors of Respiratory Failure]:

 Time from onset to admission < 7 days

 Inability to Cough

 Inability to Stand

 Inability to Lift Elbows

 Inability to Lift Head

  Liver Enzyme

- Non-invasive ventilation is not useful as patients remain unable to clear secretions

- Suxamethonium is Absolutely Contraindicated  Fatal Hyperkalemia

- If prolonged ventilation seems likely then early Tracheostomy may improve patient comfort and aid

in clearance of secretions

Circulation

 Adequate Circulating Volume

 Β-Blockers, Atropine and Pacemakers have been used to manage Autonomic Disturbances

Drugs and Disability (Specific Treatments):

IV Immunoglobulin (IgG):

 The initial treatment of choice

 IV 0.4mg/kg OD for 5 days

 Much more convenient than plasma exchange, same efficacy and Less Side Effects

 It should be commenced within 2 weeks of the onset of symptoms

 Side Effects (Rare): nausea, fever, headache, a transient rise in liver enzymes, encephalopathy, meningism and malaise Serious SE; skin reactions (e.g erythroderma) and hypercoagulability

 Contraindications:

*IgA deficiency (increased incidence of Anaphylaxis) and Previous anaphylaxis to

immunoglobulin therapy IgA levels must be checked in all patients prior to administration of immunoglobulin

* Renal impairment as renal function may deteriorate further with immunoglobulin therapy

*Severe congestive cardiac failure is also a relative contraindication

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Plasma Exchange:

 Involves the removal of about 200 ml/kg of plasma over 4–6 sessions and replacement with 4.5% human albumin solution

 Thought to work by removal of a humoral demyelinating factor

 This treatment does not influence mortality but reduce the duration of ventilator dependence and hospital stay, and leads to earlier mobilisation if commenced within 2 weeks of the onset of illness

 It is associated with more significant side effects and contraindications compared with

immunoglobulin therapy Administration is limited to specialist centres

 Side effects: Hypotension, hypocalcaemia, coagulation abnormalities and septicaemia

 Contraindications: Haemodynamic instability, Sepsis and severe haemostatic problems

CSF filtration

Psychotherapy

Early enteral Feeding

What Other Problems Might They Encounter On ICU?

 Autonomic Neuropathy: Ensure Adequate Circulating Volume And Sedation

Β-Blockers, Atropine And Pacemakers Have Been Used To Manage Autonomic Disturbances

 Pain Is Common (Especially In the Back and Lower Limbs) and Can Be a Major Problem Carbamazepine is Useful Adjuvant for Pain Control, Reducing Narcotic Requirements

Intensive Physiotherapy Is Essential

 GI Haemorrhage

The Prognosis:

 Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12

months

 Patients may have persistent weakness, areflexia, imbalance, or sensory loss

 Some patients may have permanent neurologic sequelae including bilateral foot drop,

intrinsic hand muscle wasting, sensory ataxia, and dysaesthesia

 The mortality rate is approximately 10%, usually from complications such as cardiac arrest secondary to autonomic dysfunction, sepsis, pulmonary embolism and respiratory infection

Poorer Prognosis Is Associated with:

 Older Patients

 Preceding Campylobacter Jejuni Infection

 Need For Mechanical Ventilation

 Rapid Progression of Symptoms

 Extensive disease

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7- Status Epilepticus

(a) What is the WHO definition of status epilepticus (SE)? How may it be classified?

(b) What are the systemic effects of SE?

(c) What are the causes of SE?

(d) Describe the pharmacological treatment options for SE

(e) Describe the non-pharmacological options for treatment SE

 The WHO definition of status epilepticus (SE):

A continuous, generalized, convulsive seizure lasting more than 5 minutes,

OR

Two or more seizures during which the patient does not return to baseline consciousness

Classification:

 The systemic effects of SE:

- CVS: early - hypertension, tachycardia; late - hypotension, bradycardia, dysrythmias

- Resp: Respiratory acidaemia, airway obstruction leading to Hypoxaemia, Hypercapnia and

Aspiration

- CNS: Increased CMR, hyperthermia, raised ICP and cerebral oedema

- Metabolic: Early: Lactic acidosis, hyperglycaemia; Late: Hypoglycaemia

- Endocrine: Increased circulating catecholamines

- Renal: Rhabdomyolysis

- Other: Trauma secondary to seizure: fractures, dental damage

 The causes of SE:

- Neurological: trauma, cerebral haemorrhage, infarction, tumours, infection (meningitis,

encephalitis)

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- Drugs:

-Poor compliance with anti-epileptic medication in known epileptics,

-Toxicity including TCAs, flumazenil, Cocaine;

-Withdrawal e.g from alcohol

- Electrolyte disorders e.g hypoNa, hypoglycaemia, hypoCa, hypoMg

- 3rd line: - Anaesthetic agents as IV bolus +/- continuous infusion

- 1st line: Benzodiazepines

-Diazepam can also be given rectally if IV access not

established, or Buccal midazolam

-These work by increasing GABA-mediated cerebral

inhibition, decreasing seizure threshold

cardiovascular monitoring (can cause

hypotension/bradycardia); Sodium Valproate as IV bolus

followed by infusion; Levetiracetam as IV bolus

- 3rd line: - Anaesthetic agents as IV bolus +/- continuous infusion

+/- 5-10mg/kg/hr infusion; N.B hypotension, bradycardia, be aware of propofol infusion syndrome with prolonged infusion or paediatric population

suppression of neuronal activity, detected on EEG IV bolus 3-7mg/kg, +/- 3-5mg/kg/hr continuous infusion

**N.B These are usually accompanied by a neuromuscular blocking agent in order to facilitate tracheal intubation for the purpose of airway protection

-Neuromuscular blocking agents may stop overt seizure activity but patient may continue to have NCSE

*N.B In the case of the eclamptic fit, first line treatment is 4g MgSO4 IV over 15minutes, followed by infusion as necessary Benzodiazepines and other anti-epileptics are not used in this scenario

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The non-pharmacological options for treatment SE

- Use safe ABCDE approach

Supportive care includes airway maintenance and protection with opening manouvres, recovery position to avoid aspiration, adjuncts or formal protection with intubation via a cuffed, ETT

infection considered likely, if known cerebral tumour consider IV dexamethasone to reduce swelling

neurogenic pulmonary oedema or raising ICP);

Vasopressor agents can be used to prevent fluid overload

- Ensure patient is not at risk of injuring themselves or others whilst actively seizing

- Aim to achieve and maintain normothermia

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