Renal Support in the Critically Ill

The second Renal Support in the Critically Ill Conference, hosted by The Alfred ICU, took place last week.

Here are the top 10 ‘take home messages’ from the conference:


1. Biomarkers
Biomarkers of structural kidney injury, such as Neutrophil gelatinase-associated lipocalin (NGAL), are becoming more widely available. Early measurement of these biomarkers predicts development of acute kidney injury (AKI) and associated adverse outcomes.


2. Renal recovery
Renal recovery from AKI is influenced by a number of factors; severity, duration, CKD status, and patient age and comorbidity. Data suggest that initial application of continuous renal replacement therapy (CRRT) – as compared to intermittent RRT (IRRT) – may improve the likelihood of complete recovery (e.g. free from chronic dialysis).

3. Fluids and renal perfusion pressure
IV fluids do not lead to a sustained increase in renal blood flow (RBF) and do not increase renal perfusion pressure in large animal models of sepsis. Their use in response to oliguria may lead to a positive fluid balance, which has been associated with adverse outcomes in the critically ill. Use of vasopressors to improve perfusion pressure (in reference to the patient’s baseline blood pressure) may prove a more optimal approach.

4. Drug pharmacokinetics
Drug pharmacokinetics are significantly altered in critically ill patients, in part due to alterations in renal clearance associated with AKI. Application of CRRT further complicates this process, such that therapeutic drug monitoring offers the best method of optimizing drug exposure.

5. Citrate anticoagulation for RRT
Citrate offers an attractive alternative to heparin for circuit anticoagulation, and appears to prolong filter lifespan. Caution remains when applying this therapy in patients with hepatic failure.

6. Loop diuretics
Data on loop diuretic therapy in patients with AKI remains conflicted. These agents remain a consideration in the management of fluid overload, and the lack of an adequate diuresis in response to loop diuretics, may serve as a useful trigger to commence RRT.

7. Septic AKI
Animal data suggests there is neither a significant deterioration in RBF, nor any significant structural abnormality in models of septic AKI. The noteworthy disparity between functional and structural characteristics in this setting suggests an otherwise unknown mechanism.

8. Synthetic colloids and Saline
Hydroxyethyl starch (HES) is clearly associated with AKI, while there is very little data on the safety of other synthetic colloids in the critically ill. Chloride rich solutions (0.9% saline) cause a reduction in RBF in animal models, and renal cortical perfusion in healthy volunteers. Decreasing chloride administration may decrease renal dysfunction.

9. Initiation of RRT
Initiation of RRT in ICU is a complex process, such that there is a poor understanding of the standard of care delivered across centers. Earlier initiation of RRT may have clinical benefits, although the quality of existing data is poor.

10. ECMO and renal failure
Extracorporeal membrane oxygenation (ECMO) initiated after renal failure is associated with reduced survival. RRT can be safely provided in such patients by accessing the ECMO circuit.

 

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Best Case Ever 23 Stuart Swadron – The Effect of Medical Insurance on ED Care

EM Cases brings you Canada's brightest minds in Emergency Medicine. Dr. Stuart Swadron, EM:RAP's 'Captain Cortex' in fact went to medical school at the University of Toronto and practiced in British Columbia before he headed down to Los Angeles to complete his Emergency Medicine Residency and become the residency program director at USC. So he is just the man to tell us his Best Case Ever about The Effect of Medical Insurance on ED Care and highlight some of the differences between the U.S. and Canadian health care systems. This is in anticipation of our upcoming EM Cases episode on North York General's 'Highlights of the Emergency Medicine Update Conference 2014', Canada's largest and best EM Conference where Dr. Swadron spoke eloquently about his approach to Vertigo in the ED including the value of the HINTS exam. In this upcoming episode we will also have Dr. Amal Mattu talking about the most important Cardiology Literature from the past year. We would love to hear your opinion on how the Canadian and U.S. health care systems could be changed to help improve patient care in our emergency departments. Please post your comments below.

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Garrapata en conducto auditivo

Escolar de diez años consulta por otorragia con manejo previo por dos colegas con amoxicilina más ácido clavulanico por 14 días e ibuprofeno 400 mg para el dolor realizo examen físico cae con abundante sangrado se aprecia cuerpo extraño y proceso con clic haciendo palanca a retirarlo y obtengo esto


Una garrapata la madre se me enoja diciendo que "como va a ser garrapata" así que lo envíe a estudio histopatologico ,


Mostrando image.jpeg
 Esperamos la resolución de este interesante caso de Dr Hector Zambrano

Own the Immunosuppressants!

Five minute teaching 001

Author: Paul Nixon
Reviewer: Chris Nickson

If you’re looking after transplant patients in the ICU, it is critical that you get the immunosuppression right. You need to OWN THE IMMUNOSUPPRESSANTS!

At The Alfred ICU we have a regular 5 minute teaching session that covers the basics of transplant immunosuppression. If you can answer the questions below, you’ll be on your way to becoming a transplant immunosuppression guru.

Q1. Why is immunosuppression used?

Required post-transplantation to prevent both

  • Acute humoral rejection (B cell antibody mediated)
  • Chronic cell mediated rejection (T cell mediated)

Q2. What types of immunosuppressant drugs are used?

Almost always 3 classes of immunosuppressive drugs are used simultaneously!

  1. Corticosteroids
  2. Anti-metabolites (e.g. azithioprine, mycophenolate)
  3. Calcineurin inhibitors (CNI) (e.g. tacrolimus, cyclosporin)

Q3. How are they given?

Loading dose prior to theatre

  • oral dose of anti-metabolite
  • oral dose of CNI (if renal function ok)

Loading dose in theatre

  • 2 x 500mg methylprednisolone IV

Maintenance doses

  • Corticosteroid
    - Tapering dose of methylprednisolone / prednisolone over 2 weeks
    - Usually remain on ~ 20mg / day
  • Mycophenolate / Azathioprine
    - IV dosing until absorbing feeds then transition to oral
    - Mycophenolate BD dosing
    - Azathioprine daily dosing
  • CNI
    - IV dosing until absorbing feeds then transition to oral
    - BD dosing

Q4. What are some other options if a CNI is contraindicated or if the patient is intolerant of CNIs?

If a CNI is contraindicated (eg. pre-existing kidney disease):

  • Basiliximab (Simulect) can be used
  • This is a monoclonal antibody that has taken over the role of ATGAM

When patients are intolerant of CNI:

  • Occasionally a proliferation inhibitor is used
  • Everolimus or sirolimus

Q5. What are the important side effects of the different immunosuppressant drugs?

All classes

  • opportunistic infections
  • common hospital acquired infections

Corticosteroids

  • hyperglycaemia
  • hypertension
  • osteoporosis (chronic use)
  • peptic ulcers

Calcineurin inhibitors – tacrolimus and cyclosporin

  • acute kidney dysfunction
  • electrolyte disturbance (low magnesium)
  • diabetes mellitus
  • hyperlipidaemia
  • neurological disturbance including seizures and posterior reversible encephalopathy syndrome (PRES)

Mycophenolate

  • gastrointestinal disturbance

Azithioprine

  • leucopaenia
  • gastrointestinal disturbance
  • hepatitis and pancreatitis

Q6. How do these immunosuppressant drugs work?

The short and highly simplified answer is that, essentially, they all block signalling from T cell to T cell and between T cells and B cells, and they  target some point in the IL-2 signalling pathway.

Immunologic mechanisms leading to graft rejection and sites of action of immunosuppressive drugs are shown in this figure from Lindenfeld et al, 2004.

References and Links

  • Lindenfeld J, Miller GG, Shakar SF, Zolty R, Lowes BD, Wolfel EE, Mestroni L, Page RL 2nd, Kobashigawa J. Drug therapy in the heart transplant recipient: part I: cardiac rejection and immunosuppressive drugs. Circulation. 2004 Dec 14;110(24):3734-40. Review. PubMed PMID: 15596559. [Free Full Text]

The post Own the Immunosuppressants! appeared first on INTENSIVE.

Own the Immunosuppressants!

Five minute teaching 001

Author: Paul Nixon
Reviewer: Chris Nickson

If you’re looking after transplant patients in the ICU, it is critical that you get the immunosuppression right. You need to OWN THE IMMUNOSUPPRESSANTS!

At The Alfred ICU we have a regular 5 minute teaching session that covers the basics of transplant immunosuppression. If you can answer the questions below, you’ll be on your way to becoming a transplant immunosuppression guru.

Q1. Why is immunosuppression used?

Required post-transplantation to prevent both

  • Acute humoral rejection (B cell antibody mediated)
  • Chronic cell mediated rejection (T cell mediated)

Q2. What types of immunosuppressant drugs are used?

Almost always 3 classes of immunosuppressive drugs are used simultaneously!

  1. Corticosteroids
  2. Anti-metabolites (e.g. azithioprine, mycophenolate)
  3. Calcineurin inhibitors (CNI) (e.g. tacrolimus, cyclosporin)

Q3. How are they given?

Loading dose prior to theatre

  • oral dose of anti-metabolite
  • oral dose of CNI (if renal function ok)

Loading dose in theatre

  • 2 x 500mg methylprednisolone IV

Maintenance doses

  • Corticosteroid
    - Tapering dose of methylprednisolone / prednisolone over 2 weeks
    - Usually remain on ~ 20mg / day
  • Mycophenolate / Azathioprine
    - IV dosing until absorbing feeds then transition to oral
    - Mycophenolate BD dosing
    - Azathioprine daily dosing
  • CNI
    - IV dosing until absorbing feeds then transition to oral
    - BD dosing

Q4. What are some other options if a CNI is contraindicated or if the patient is intolerant of CNIs?

If a CNI is contraindicated (eg. pre-existing kidney disease):

  • Basiliximab (Simulect) can be used
  • This is a monoclonal antibody that has taken over the role of ATGAM

When patients are intolerant of CNI:

  • Occasionally a proliferation inhibitor is used
  • Everolimus or sirolimus

Q5. What are the important side effects of the different immunosuppressant drugs?

All classes

  • opportunistic infections
  • common hospital acquired infections

Corticosteroids

  • hyperglycaemia
  • hypertension
  • osteoporosis (chronic use)
  • peptic ulcers

Calcineurin inhibitors – tacrolimus and cyclosporin

  • acute kidney dysfunction
  • electrolyte disturbance (low magnesium)
  • diabetes mellitus
  • hyperlipidaemia
  • neurological disturbance including seizures and posterior reversible encephalopathy syndrome (PRES)

Mycophenolate

  • gastrointestinal disturbance

Azithioprine

  • leucopaenia
  • gastrointestinal disturbance
  • hepatitis and pancreatitis

Q6. How do these immunosuppressant drugs work?

The short and highly simplified answer is that, essentially, they all block signalling from T cell to T cell and between T cells and B cells, and they  target some point in the IL-2 signalling pathway.

References and Links

  • Lindenfeld J, Miller GG, Shakar SF, Zolty R, Lowes BD, Wolfel EE, Mestroni L, Page RL 2nd, Kobashigawa J. Drug therapy in the heart transplant recipient: part I: cardiac rejection and immunosuppressive drugs. Circulation. 2004 Dec 14;110(24):3734-40. Review. PubMed PMID: 15596559. [Free Full Text]

The post Own the Immunosuppressants! appeared first on INTENSIVE.