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  • play_arrowPleural Effusion & Empyema
    Dr Swapnil Pawar Pleural Effusion

Written by Dr Ashly Liu

A pleural effusion is a pathological fluid collection between the parietal and visceral pleura.

A parapneumonic effusion is a pleural effusion associated with adjacent pneumonia. It may occur in up to 50% on pneumonia cases.

  • A simple parapneumonic effusion is a non-loculated transudate that is sterile.
  • A complicated parapneumonic effusion is an effusion that has been infected with bacteria/microorganisms. This may refer to a loculated effusion or empyema, with changes in the pleural fluid due to bacterial invasion of the pleural space.

An empyema refers to a collection of pus within the pleural space, which can develop when pyogenic bacteria invade the pleural space from adjacent pneumonia, direct inoculation (eg, from blunt trauma) or other sources.

Light’s Criteria

Management of Parapneumonic Effusion

Ideally, we would collect pleural fluid samples for culture to identify the pathogen. The most common pathogens for empyema are: streptococcus pneumoniae, Staphylococcus aureus, and Group A Streptococcus are the most common causes of empyema.

Empirical antibiotics (as per eTG):

  • Low to moderate disease – benzylpenicillin 1.2g QID + Metronidazole 500mg BD
  • High severity disease – ceftriaxone 2g daily + Metronidazole 500mg BD

Uncomplicated parapneumonic effusion – Antibiotics

As parapneumonic effusions are initially sterile and a complication of pneumonia, management is primarily intravenous antibiotics. Duration is dependent on clinical presentation and hospital guidelines. For simple parapneumonic effusions, they after usually treated with 1-2 weeks of antibiotic therapy.

For clinically significant parapneumonic effusions (e.g. depth greater than 10mm on lateral decubitus XR, greater than 30mm on CT, dyspnoea attributable to effusion), they require diagnostic pleural fluid sampling and MCS.

If parapneumonic effusions are left undetected and untreated, it may develop into a complicated pleural effusion or empyema.

Complicated pleural effusion and empyema – Antibiotics + Drainage

Duration of antibiotics would be dependent on clinical presentation and radiographic response, complicated parapneumonic effusions are often treated for 2-3 weeks and empyemas can be for up to 4-6 weeks of antibiotic therapy.

Prompt drainage of the pleural effusion is indicated in empyemas, loculated pleural effusions and positive pleural fluid gram stain or culture. This insertion of an intercostal catheter drain, they are usually performed by ultrasound or CT guidance. Drains typically remain until drain output is minimal for 2-3 days (assuming nil blockages) and there is a reasonable reduction of effusion.

Once the patient is clinically stable, and there is a reasonable reduction in pleural effusion, they are often discharged on oral antibiotics, and an outpatient follow-up CT chest to confirm the resolution

When treatment fails

  • Conservative treatment
  • Intrapleural fibrinolysis therapy (twice daily for 3 days)
    • Mix alteplase 10mg + dornase alfa 5mg in 50mL of sodium chloride 0.9% and inject via intercostal tube.
    • The tube is clamped for 2 hours and then unclamp.
    • It may require suction (dependent on hospital guidelines) and analgesia
  • VATS (video-assisted thoracic surgery) or thoracotomy – performed by cardiothoracic surgery

UpToDate “Management and prognosis of parapneumonic pleural effusion and empyema in adults.”

UpToDate “Diagnostic evaluation of the hemodynamically stable adult with a pleural effusion.”

UpToDate “Pleural fluid analysis in adults with a pleural effusion

eTG “Pleural effusion in adults”

eTG “Parapneumonic effusion and empyema”

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  • play_arrowObstructive Sleep Apnea
    Dr Swapnil Pawar Obstructive Sleep Apnoea

Written by Dr Andrew Lam

Diagnosis and Severity of OSA

OSA confirmed by sleep study by the apnoea hypopnoea index (AHI), which represents the number of apnoeas/hypopnoeas detected in 1 hour.

Diagnosis of OSA made if:

AHI > 15 in an asymptomatic patient

AHI > 5 in symptomatic patient

Mild OSA: AHI > 5 but < 15

Moderate OSA: AHI > 15 but < 30

Severe OSA: AHI > 30

Epworth Sleepiness Scale

In the following situations, how likely are you to fall asleep?

0 – No chance

1 – Slight chance

2 – Moderate chance

3 – High chance

| Situation | Chance of Falling Asleep (0-3) | | Sitting and Reading | | Watching TV | | Sitting inactive in a public place | | As passenger in the car for an hour without break | | Sitting and talking to someone | | Sitting quietly after lunch without alcohol. | | In a car, while stopped for a few minutes for traffic |

0-7: Unlikely to be abnormally sleepy

8-9: Average amount of daytime sleepiness

10-15: May be excessively sleepy depending on the situation. Consider seeking medical attention

16-24: Excessively sleepy and should consider seeking medical attention.

STOP-BANG Questionnaire

S – Snoring? (Can be heard through closed doors)

T – Tired? (Feel tired, sleepy or fatigued in the daytime)

O – Observed choking/gasping in sleep?

P – Pressure (Treated for or have hypertension)

B – BMI > 35?

A – Age > 50?

N – Neck size (Collar size >40cm)

G – Gender? (Male at higher risk)

Low Risk: Score 0-2

Intermediate Risk: Score 3-4

High Risk: Score 5-8

Complications

Cardiovascular: Hypertension, LV Failure/Hypertrophy, Myocardial Ischaemia, Arrhythmias.

Thought to be secondary to a combination of hypoxia/hypercapnia and episodes of sympathetic drive/oxidative stress associated with this.

Pulmonary: Pulmonary hypertension and subsequent right sided heart strain/failure. Thought to be due to reflexive pulmonary vasoconstriction during episodes of hypoxis

Neuropsychiatric: Decreased executive and cognitive function, mood disorders, psychosis, memory deficits

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  • play_arrowSpinal Cord Compression
    Dr Swapnil Pawar Spinal Cord CompressionWritten by – Ashly LiuSpinal Cord Compression Shownotes

Spinal cord compression is when arterial, venous and cerebrospinal fluid spaces or the cord are compressed or displaced.

Differentials include

  • Trauma including MVA, falls, and osteoporotic fractures.
  • Intervertebral disc herniation
  • Malignancy, including metastases
  • Spinal epidural abscess

Common Presentation

Patients can present in a variety of ways depending on the level of the spine that is affected.

The typical clinical findings of pain, sensory changes (numbness and paraesthesia) and motor changes (weakness or paralysis) can be seen in most forms of spinal compression. Other signs also include hyperreflexia and sphincter dysfunction (urinary or anal). Concerning signs would be an acute onset of pain or bowel/bladder changes.

Risk factors

  • Trauma – motor vehicle accident or high-risk sports activities
  • History of malignancy
  • Immunosuppression
  • Intravenous drug use

Red Flags: Acute onset and duration of symptoms

Investigations

The diagnostic investigation for spinal cord compression is an MRI spine.

Management

Trauma

  1. Immobilisation with a cervical collar, including trauma review
  2. For confirmed spinal injury, urgent neural decompression and spinal stabilisation (within 24 hours)
  3. Management of complication
    1. DVT prophylaxis
    2. Autonomic dysfunction +/- prevention of hypotension
    3. Prevention of stress ulceration with PPI for at least four weeks
    4. Nutritional support

Intervertebral disc compression

  1. Emergency neurosurgery surgery for spine decompression (within 48 hours after onset of symptoms.
  2. Management of complication
    1. DVT prophylaxis
    2. Autonomic dysfunction +/- prevention of hypotension
    3. IDC + laxatives for bowel and bladder dysfunction
    4. Prevention of stress ulceration with PPI for at least four weeks
    5. Nutritional support
    6. Pressure injury prevention

Malignant Spine compression

  1. Analgesia + bowel/bladder management with IDC
  2. Corticosteroids
  3. Decompressive laminectomy/vertebrectomy and/or radiotherapy

Epidural abscess

  1. IV antibiotics depending on the pathogen (S. aureus, Strep, Pseudomonas, E. Coli, Mycobacterium TB)
  2. Surgery with cord decompression, including tissue sampling
    1. For less disabling symptoms, CT-guided needle aspiration of lesions

References

BMJ – Spinal Cord Compression “https://bestpractice.bmj.com.acs.hcn.com.au/topics/en-gb/1012”

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play_arrow Lithium Toxicity Dr Swapnil Pawar Lithium Toxicity Written by Dr Andrew Lam Interpretation of Lithium Levels Therapeutic level – 0.8 – 1.2mmol/L Mild Toxicity – 1.5 – 2.5mmol/L Moderate to Severe Toxicity from – 2.5 – 3.5mmol/L  Severe toxicity – >3.5mmol/L Symptoms of Toxicity  Gastrointestinal – nausea, vomiting and [...]

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play_arrow Ectopic Pregnancy Dr Swapnil Pawar Ectopic Pregnancy  Written by Dr Ashley Liu Ectopic Pregnancy Ectopic pregnancies should always be considered in any patient of reproductive age with vaginal bleeding +/- abdominal pain. Clinical Manifestation The most common presentation of ectopic pregnancy is usually first-trimester vaginal bleeding and/or abdominal pain. [...]

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play_arrow Post Partum hemorrhage Dr Swapnil Pawar     Post-Partum Haemorrhage Blog written by – Dr Andrew Lam   Criteria for PPH: Cumulative blood loss >1L OR bleeding with signs/symptoms of hypovolemia within 24 hours of delivery Criteria remain the same, regardless of route of birth Causes of PPH: Uterine [...]

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play_arrow Supra-ventricular Tachycardia Dr Swapnil Pawar Supraventricular Tachycardia Blog written by – Dr Ashly Liu Summary If unstable: (1) ELECTRICITY (2) Pharmacology If stable: (1) Vasovagal manoeuvres  (2) Pharmacology (3) ELECTRICITY (if unstable) Is the patient stable or unstable? Primary Survey to assess for haemodynamic instability Airway: airway maneuvers (chin [...]

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play_arrow Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) Dr Swapnil Pawar SJS/TEN Shownotes   Written by Dr Andrew Lam   SJS – Skin detachment affecting <10% of body surface area TEN – Skin detachment affecting >30% of body surface area SJS/TEN Overlap Syndrome – Skin detachment affecting 10-30% of [...]

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play_arrow Rhabdomyolysis Dr Swapnil Pawar   This week’s case presentation focuses on Rhabdomyolysis – history, examination and investigations. We discuss specific life-threatening complications to watch out for and the ongoing monitoring required for signs of acute kidney injury.                  

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play_arrow Medspresso #Episode 51: Asthma Dr Swapnil Pawar Asthma Written by Dr Andrew Lam   Classification of Asthma Severity Mild/Moderate Severe Life Threatening O2 Saturations >94% 90-94% <90% Auscultation Wheeze May be similar to mild/moderate Silent chest Speech Can finish a sentence Phrases Single words Respiratory Distress Minimal Some use [...]

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play_arrow Status Epilepticus Dr Swapnil Pawar Status Epilepticus Blog written by Dr Ashly Liu Definition A seizure that lasts longer than 5 minutes, or having more than 1 seizure within a 5 minutes period, without returning to a normal level of consciousness between episodes is called status epilepticus.  Approach to [...]

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Abdominal Aortic Aneurysm play_arrow Abdominal Aortic Aneurysm Dr Swapnil Pawar Blog Written by Dr Andrew Lam Risk Factors for AAA Age Gender (Males more at risk) Smoking Atherosclerosis Hypertension Connective Tissue Diseases (i.e. Marfan’s, Ehlers-Danlos) Family history of AAA Open AAA Repair vs. Endovascular Repair   Open AAA Repair Endovascular [...]

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play_arrow Hypocalcemia Dr Swapnil Pawar Hypocalcaemia Written by – Dr Ashly Liu Calcium Serum calcium is normally maintained in a narrow range that’s required for optimal activity of extra and intracellular processes. Where is it in our body? Calcium is typically transported partly bound to plasma proteins (i.e. albumin), to [...]

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play_arrow Neurolept Malignant Syndrome Dr Swapnil Pawar Neuroleptic Malignant Syndrome Clinical Features of NMS Altered mental state: Agitated delirium with confusion, and can sometimes present as catatonia and mutism. Progresses to stupor and coma Muscular Rigidity: Often presents as lead pipe rigidity, but may appear cogwheeling if there is superimposed [...]

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play_arrow Haemtemesis Dr Swapnil Pawar Scoring systems in upper GI bleeds Scoring systems are helpful in identifying patients who are low risk for rebleeding or mortality, and therefore can be considered for outpatient management Glasgow-Blatchford Score  Glasgow Blatchford Score does not take endoscopic data into account so it can be [...]

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play_arrow TCA Overdose Dr Swapnil Pawar TCA Toxicity  Blog Written by Dr Andrew Lam ECG Findings in TCA Toxicity Tachycardia Widened QRS Complex Deep S wave in Lead I and AvL Tall R wave in AvR In severe toxicity may also manifest as VF or VT Management of TCA Toxicity [...]

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play_arrow Septic Arthritis Dr Swapnil Pawar Blog Written by Dr Ashley Liu Septic Arthritis Differentials for Mono-arthritis Infective (i.e. septic arthritis) History: ·   Hot, swollen singular joint ·   Constitutional symptoms (high-grade fever, malaise, weight loss) Exam: ·   Inability to weight bear Diagnostic investigation: Joint aspirate ·   [...]

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play_arrow A-V Blocks Dr Swapnil Pawar Atrioventricular Blocks Written by Dr Andrew Lam First Degree Heart Block  Prolongation of the PR interval (>200ms) Benign as an isolated entity that doesn’t cause haemodynamic instability. Intervention generally not required Second Degree Heart Block (Mobitz Type 1 – Wenckebach) Progressive prolongation of the [...]

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play_arrow Paracetamol Overdose Dr Swapnil Pawar Paracetamol Overdose Written by Dr Andrew Lam Clinical Stages of Paracetamol Overdose Stage I (0-24 hours) – relatively non-specific with nausea, vomiting, malaise and diaphoresis, though some patients may be asymptomatic. Uncommonly may have CNS depression Stage II (24-72 hours) –  resolution of initial [...]

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play_arrow Gout Dr Swapnil Pawar Written by – Dr Andrew Lam Gout vs. Pseudogout Gout Pseudogout Predominant Sites Affected Small Joints (i.e. 1st MTP) Large Joints (i.e. knee) Clinical Findings Marked swelling, erythema and tenderness +/- tophi Swelling and tenderness often less marked than in gout Pathophysiology Uric acid crystal [...]

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play_arrow Diverticulitis Dr Swapnil Pawar Diverticulitis Hinchey Classification Stage 0 – Clinically mild diverticulitis with just colonic wall thickening on the CT Stage 1a – Pericolic inflammation or phlegmon, and pericolic tissue changes on CT Stage 1b – Evidence of formation of a pericolic or mesocolic abscess Stage 2 – [...]

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play_arrow Pre-Eclampsia Dr Swapnil Pawar Pre-Eclampsia Blog Written by Dr Andrew Lam Hypertensive Disorders of Pregnancy Gestational Hypertension Blood Pressure >140/90 after 20 weeks gestation in a usually normotensive woman No proteinuria No evidence of end-organ damage Pre-Eclampsia Blood Pressure >140/90 after 20 weeks gestation in a usually normotensive woman [...]

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Aortic Stenosis

Dr Swapnil Pawar

Aortic Stenosis Blog written by Dr Andrew Lam Clinical Characteristics of Mitral Regurgitation vs. Aortic Stenosis

| Aortic Stenosis | Mitral Regurgitation | | Character | Crescendo-Decrescendo Mid-Systolic Murmur | Pan-Systolic Murmur | | Radiation | To Carotids | To Axilla | | Location of Greatest Intensity | R. Upper Sternal Border | 5th Intercostal Space, Mid-Clavicular Line | | Variation With Respiration | Louder on expiration, softer on inspiration | Louder on expiration, softer on inspiration |

Grading of Aortic Stenosis

Stage A (At Risk of Aortic Stenosis) – asymptomatic patients who are at risk of aortic stenosis (i.e. bicuspid aortic valve or aortic sclerosis)

Stage B (Progressive Aortic Stenosis) – asymptomatic patients with mild-moderate disease

Stage C (Asymptomatic Severe Aortic Stenosis) – patients with findings suggestive of severe valve obstruction, but still remain asymptomatic

Stage D (Symptomatic Severe Aortic Stenosis) – Patients with severe valve obstruction but clinically also exhibit symptoms

Complications of Aortic Stenosis

Heart Failure

Left ventricular hypertrophy is common in the context of aortic stenosis. Consequently, patients develop diastolic heart failure, often with preserved ejection fractions. Due to increased diastolic pressures, patients can also develop pulmonary hypertension

Arrhythmias

Patients have an increased risk of ventricular and supraventricular arrhythmias, thought to be secondary to LV hypertrophy

Sudden Cardiac Death

The mechanism is not well established but appears to be reduced following valve replacement. Annual risk for severe asymptomatic AS is 1%, but for those with severe, symptomatic AS, rates range from 8-34%.

Endocarditis

Risk increases particularly in those with congenital abnormalities (i.e. bicuspid aortic valve)

Heyde Syndrome

A syndrome involving gastrointestinal bleeding from angiodysplasia in the context of aortic stenosis. Thought to be due to the high velocity of blood in aortic stenosis resulting in unravelling of von-Willebrand Factor that inhibits its function, and hence, promotes bleeding

References:

Otto, C.M. (2021) Clinical manifestations and diagnosis of aortic stenosis in adults. UpToDate. Retrieved 18th September 2021 from https://www.uptodate.com.acs.hcn.com.au/contents/clinical-manifestations-and-diagnosis-of-aortic-stenosis-in-adults

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Ascending Cholangitis

Dr Swapnil Pawar

Ascending Cholangitis

Cholelithiasis: Presence of gallstones within the gallbladder

Choledocholithiasis: Presence of gallstones within the bile ducts

Cholecystitis: Inflammation of the gallbladder

Cholangitis: Inflammation of the bile duct system

Clinical Signs of Ascending Cholangitis

Charcot’s Triad

  • Fever
  • Jaundice
  • Right Upper Quadrant Abdominal Pain

Reynold’s Pentad

  • The 3 Symptoms of Charcot’s Triad
  • Hypotension
  • Confusion

Causes of Biliary Obstruction

Intraluminal:

  • Choledocholithiasis
  • Biliary Strictures (Post-Infectious, autoimmune, congenital)
  • Malignancy (i.e. cholangiocarcinoma)

Extraluminal:

  • Malignancy (pancreatic or duodenal carcinoma)
  • Pancreatitis (from oedema from surrounding pancreatic tissue)
  • Mirizzi Syndrome (Obstruction of the biliary tree through gallstone impacted in the cystic duct)
  • Lemmel Syndrome (Obstruction of the biliary tree through duodenal diverticula)

Risk Factors for Biliary Stone Formation

Fair – more common in Caucasian patients

Fat – patients who are obese (BMI >30) or hyperlipidaemia

Female

Fertile – for women who have had one or more children

Forty – Age > 40

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Renal Calculus

Dr Swapnil Pawar

Renal Calculus The blog is written by Dr Andrew Lam Management of Renal Calculi

Reasons for admission:

– Inability to tolerate oral intake due to nausea and vomiting

– Uncontrollable pain

– Fever

For all renal calculi:

Regular analgesia, often requiring NSAID’s and opiates

Anti-emetics if nauseous and vomiting

Advised patient to strain when voiding to encourage the passing of the stone

If <5mm – appropriate for outpatient management

If 5-10mm – appropriate for outpatient management. Tamsulosin can be commenced to encourage spontaneous passage of stone

If >10mm – Unlikely to pass spontaneously, and hence, urological referral for surgical intervention is advised

If stones <10mm do not pass spontaneously within 4 weeks, then urological input is also advised. Potential options for surgical input include:

– Shock Wave Lithotripsy

– Ureteroscopy with lithotripsy

– Percutaneous nephrolithotomy

In rare cases – laparoscopic stone removal may be indicated

At any point in time, if the patient spikes fevers or becomes septic, then urgent urology referral is warranted for a stent or nephrostomy for decompression

Prevention of Renal Calculi

For all stones, recommended measures include:

– Increased fluid intake to decrease the concentration of urine and hence, risk of precipitation

– Weight loss

– Decreased sodium intake

– Increased fruit and vegetable intake

Additional measures can be considered depending on the composition of the stone:

Calcium oxalate/phosphate

– Maintaining adequate calcium in diet (hypocalcemia worsens risk)

– Reduce animal protein intake

– Limit sucrose and fructose intake

Uric Acid

– Alkalinisation of urine

– Uric acid-lowering therapy (i.e. xanthine oxidase inhibitor)

Cystine

– Alkalinisation of urine

– Thiol containing drugs (i.e. tiopronin, D-penicillamine)

Struvite

– Antimicrobial therapy

– Urease inhibitors

References:

Curhan, G.C., Aronson, M.D., Preminger, G.M. (2021) Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis. UpToDate. Retrieved 28th August 2021 from https://www.uptodate.com.acs.hcn.com.au/contents/kidney-stones-in-adults-diagnosis-and-acute-management-of-suspected-nephrolithiasis

Curhan, G.C. (2021) Kidney stones in adults: Prevention of recurrent kidney stones. UpToDate. Retrieved 28th August 2021 from https://www.uptodate.com.acs.hcn.com.au/contents/kidney-stones-in-adults-prevention-of-recurrent-kidney-stones

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