Tag Archives: critical care

A New Algorithm to Differentiate Salt-wasting Syndrome from SIADH

In cerebral salt-wasting (CSW), natriuretic factor is produced in response to a central insult.  Natriuretic factor decreases sodium transport in proximal renal tubule which leads to urinary loss of sodium (and water) and depletion of extracellular volume.  Hypovolemia then triggers secretion of ADH, renin and aldosterone, which provides a negative feedback to decrease secretion of natriuretic factor.

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Differentiating CSW from syndrome of inappropriate antidiuretic hormone (SIADH) is problematic, laboratory work-up (urine and plasma sodium levels and urine and plasma osmolarity) is similar in both conditions.  CSW patients are usually volume depleted while SIADH patients are euvolemic.  The traditional approach of examining patient clinically to to determine volume status is inaccurate.

An interesting paper published in 2014 suggested a new algorithm to differentiate SIADH from CSW based on the effect of sodium correction on the fractional excretion of urate (FEUa).  FEurate is calculate using the folllowing formula:

c

 

Expanded:

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Another formula:

4.jpg

 

Normal FEUa = 4-11%, SIADH & CSW FEUa = >11%.  FEUa determines the percent excertion of the filtered load of urate at the glomerulus.

In SIADH, FEUa normalizes after correction of hyponatremia (see graph below):

a

whereas in CSW, FEUa remains elevated >11% after correction of hyponatremia.  The reason is probably because natriuretic factor also decreases urate transport in the proximal tubule.

b.JPG

 

Based on this finding, the paper suggests a new algorithm for determining the etiology of hyponatremia that omits reliance of UNa (and also plasma renin, aldosterone, atrial or brain antriuretic peptide, BUN/creatinine ratio).

d.JPG

Based on this algorithm, a patient with hyponatremia should undergo correction of sodium by any means (water restriction or isotonic / hypertonic saline). Observing whether FEUa normalizes or remains increased would differentiate SIADH from CSW syndrome.

 

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Reference:

Maesaka, J., Imbriano, L., Mattana, J., Gallagher, D., Bade, N. and Sharif, S. (2014). Differentiating SIADH from Cerebral/Renal Salt Wasting: Failure of the Volume Approach and Need for a New Approach to Hyponatremia. Journal of Clinical Medicine, 3(4), pp.1373-1385.

 

 

Stanford Antibiogram

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Stanford Antibiogram

 

Reference:

Errolozdalga.com. (2018). [online] Available at: http://errolozdalga.com/medicine/pages/OtherPages/shcAntibiogram2010.pdf [Accessed 6 Nov. 2018].

Venous Blood Gas – VBG-ABG correlation

Venous blood gas can be used toestimate systemic CO2 and pH levels.

Possible sites of VBG:

  1. peripheral venous sample (from venipuncture)
  2. central venous sample (from central venous catheter)
  3. mixed venous sample (from distal port of PAC)

Values from VBG:

  1. PvO2 – venous oxygen tension
  2. PvCO2 – venous carbon dioxide tension
  3. pH
  4. SvO2 – oxyhemoglobin saturation
  5. HCO3 – serum bicarbonate

PvCO2, pH, HCO3 – assess ventilation and/or acid-base status

SvO@ – guides resuscitation

PvO2 – no value

 

Correlations:

  1. Central venous sample
    1. pH – 0.03 to 0.05 pH units lower than arterial pH
    2. PvCO2 – 4-5 mm Hg higher than PaCO2
    3. HCO3 – little or no increase
  2. Mixed venous sample – similar tocentral venous sample
  3. peripheral venous sample
    1. pH – 0.02 to 0.04 pH units lower than arterial pH
    2. HCO3 –  1-2 mEq/L higher
    3. PvCO2 – 3-8 mm Hg higher than PaCO2

*varies with hemodynamic stability

 

Reference:

Uptodate.com. (2018). UpToDate. [online] Available at: https://www.uptodate.com/contents/venous-blood-gases-and-other-alternatives-to-arterial-blood-gases?search=venous%20blood%20gas&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 22 Oct. 2018].

Vertebral Artery Stenosis Studies

5 Major Studies on Treatment of VA Stenosis:

  1. CAVATAS (1997) = Carotid and Vertebral Artery Transluminal Angioplasty Study
  2. SAMMPRIS (2011) = Stenting and Aggressive Medical Management for the Prevention of Recurrent Stroke in Intracranial Stenosis
  3. VISSIT (2012) = Vitesse Intracranial Stent Study for Ischemic Therapy
  4. VAST (2013) = Vertebral Artery Stenting Trial
  5. VIST (2015) = Vertebral Artery Ischaemia Stenting Trial

*year = end of recruitment.

 

Key features of the trials comparing stenting with medical treatment which included vertebral stenosisCapture

 

Treatment:

  1. DAPT x 90d
  2. Statin
  3. BP reduction <140mm Hg
  4. Angio +/- stenting

 

Note:

  1. low perioperative complications with extracranial stenting
  2. higher risk of stroke with intracranial VA stenosis
  3. stenting = medical management for extracranial stenosis
  4. medical management better for intracranial stenosis

Capture

Powerpoint File for figure above

Reference:

Drazyk, A. and Markus, H. (2017). Recent advances in the management of symptomatic vertebral artery stenosis. Current Opinion in Neurology, p.1.

Algorithm for Treatment of Cerebral Venous Thrombosis (CVT)

An algorithm for the diagnosis and management of CVT:

Capture.JPG

CTV, CT venography; CVT, cerebral venous thrombosis; ICH, intracerebral
hemorrhage; LMWH, low molecular weight heparin; MRV, magnetic resonance venography; PRES, posterior reversible encephalopathy syndrome; UHF,
unfractionated heparin.

 

Table 1 Major risk factors and conditions associated with CVT
Infection

  • INFECTION:
    • Paranasal sinusitis
    • Intracranial infections: abscess, meningitis
    • Trauma Head trauma, neurosurgical operations
    • Internal jugular catheter
  • MEDICAL / SURGICAL CONDITIONS
    • Dehydration
    • Pregnancy and puerperium
    • Coagulation disorders: factor V Leiden, protein C / S deficiency, antithrombin III deficiency, hyperhomocysteinemia, APAS
    • Hematologic disorders: polycythemia, sickle cell disease, TTP, polycythemia, PNH
    • Malignancies, inflammatory bowel disease, nephrotic syndrome, liver cirrhosis, collagen vascular disease including SLE, Wegener’s granulomatosis and Behçet syndrome
    • Previous surgical procedures
  • MEDICATION
    • Oral contraceptives, hormone replacement therapy,  L-asparagenase, corticosteroid

 

Table 3 Clinical presentations of CVT:

  • Symptoms
    • Headache
    • Double or blurred vision
    • Altered consciousness
    • Seizure
    • Behavioral symptoms (delirium, amnesia, mutism)
  • Signs
    • Papilledema
    • Focal neurologic deficit
    • Cranial nerve palsy
    • Nystagmus

 

Society of Neurointerventional Surgery (SNIS) Recommendations:

Imaging
► A combination of MRI/MRV or CT/CTV studies should be performed in patients with suspected CVT (class I; level of evidence C).
► DSA as a diagnostic modality is indicated in cases of suspected CVT when the diagnosis of CVT cannot be reliabl established with non-invasive imaging alone (class IIa; level of evidence C).

Medical and surgical treatment
► Anticoagulation with unfractionated heparin or low molecular weight heparin is reasonable in patients with CVT (class IIa; level of evidence C).
► Decompressive craniectomy may be considered in patients with large parenchymal lesions causing herniation or intractable intracranial hypertension (class IIb; level of evidence C).

Endovascular therapy
► Endovascular therapy may be considered in patients with clinical deterioration despite anticoagulation, or with severe neurological deficits or coma (class IIb; level of evidence C). The duration of anticoagulation therapy before declaring it to be a ‘failure’ and proceeding with endovascular therapy is unknown.
► There is insufficient evidence to determine which endovascular approach and device provides the optimal restoration of venous outflow in CVT. In many cases, a variety of treatment approaches is required to establish sinus patency.

 

Radiologic Findings in CVT:

  1.  noncontrast CT – hyperdensity of occluded sinuses + cerebral edema +/- ICH
  2. contrast CT – empty delta sign, HU>70% highly specific for acute CVT
  3. MRI – T2 hypointensity in acute CVT, T1 and T2 hyperintensity in subacute CVT

 

 

References

Lee, S., Mokin, M., Hetts, S., Fifi, J., Bousser, M. and Fraser, J. (2018). Current endovascular strategies for cerebral venous thrombosis: report of the SNIS Standards and Guidelines Committee. Journal of NeuroInterventional Surgery, 10(8), pp.803-810.

 

Stress Dose Steroids

WHEN IS STRESS DOSE STEROIDS INDICATED?

  • depends on history of steroid intake and likelihood of HPA supression + type and duration of surgery
  • NONSUPPRESSED HPA AXIS: 
    • < 3 weeks of steroids at any dose
    • prednisone <5mg/daily for any duration
    • prednisone <10mg every other day
    • PLAN:  continue same regimen perioperatively; no need for cosyntropin test or stress dose steroids
  • SUPPRESSED HPA AXIS
    • prednisone >20mg/day x 3 weeks or more OR Cushingoid appearance
    • PLAN:
      • give stress dose steroids based on type and duration of surgery (see below)
  • INTERMEDIATE HPA SUPPRESSION (Unknown HPA Axis suppression, previous 3 or more intraarticular or spinal steroid injections within 3 mos prior to suregery)
    • PLAN
      • evaluate HPA axis 
        • check AM cortisol (8a.m.) after 24h off steroids
        • if <5 ug/dL – likely suppressed axis; give stress dose steroids
        • if >10 ug/dL – likely no supression; continue current dose on day of surgery
        • if 5-10 ug/dL – ACTH stim test or empiric stress dose steroids
      • ACTH stim test (standard is 250 ug):
        • if serum cortisol <18 ug/dL 30 mins after ACTH – give stress dose steroids
        • if >serum cortisol >18 ug/dL 30 mins after ACTH – no stress dose steroids

 

STEROIDS BASED ON TYPE AND DURATION OF SURGERY

MINOR PROCEDURES / LOCAL ANESTHESIA – stress dose not necessary, take AM steroids

MODERATE SURGICAL STRESS: (eg. LE revascularization, total joint replacement)

  1. take AM steroids
  2. hydrocortisone 50mg IV prior to procedure, 25mg IV q8h x 24h
  3. resums usual dose after

MAJOR SURGICAL STRESS (e.g open heart surgery, proctocolectomy, esophagogastrectomy)

  1. take AM steroids
  2. hydrocortisone 100mg IV before induction of anesthesia
  3. hydrocortisone 50mg q8h x 24h
  4. taper by half per day to maintenance dose

 

 

 

Reference:

Uptodate.com. (2018). UpToDate. [online] Available at: http://www.uptodate.com/contents/the-management-of-the-surgical-patient-taking-glucocorticoids?search=stress+dose+steroids&source=search_result&selectedTitle=1~60#H6 [Accessed 25 Mar. 2018].

Pulmonary Artery Catheter Waveforms and Normal Values

As the PAC is inserted, the following waveforms can be observed.

1. When the catheters enters the RA, a CVP tracing is seen – characterized by a and v waves.img_1652

 

 

 

 

 

 

 

 

 

2. As the catheter enters the RV, a sharp increase in systolic pressure is noted.img_1653

3. As the catheter is advanced to the pulmonary artery, an increment in diastolic pressure is seen as well as the presence of a dichromatic notch. img_1654

4. When the catheter is advanced further into the pulmonary artery, and wedged – a sine wave that oscillates with respiration is seen. img_1655

THE RA WAVEFORM:

The RA waveform is characterized by presence of 2 waves: a wave (contraction of the RA) and the v wave (passive filling of the RA).

The x descent represents RA relaxation, which is interrupted by the c wave which represents closure of the tricuspid valve.

The y descent follows the v wave, which signals the opening of the tricuspid valve and exit of blood from the RA to the RV.

img_1656

OVERDAMPING:

The wave below illustrates flushing of the catheter – which results in high pressures in the transducer (1). Flushing stops, and results in fall in pressures and an overshoot (2), and a return to normal waveform.

img_1661

The wave below – overshooting is absent, and the waveform is flattened, which is found in an overdamped waveform. Overdamping can be caused by a kinked catheter, air bubbles, fibrin clot.

img_1662

 

 

 

 

 

CATHETER WHIP.

The graph below illustrate catheter whip – where ventrcicular contractions are transmitted to the PAC.

img_1663

OVERWEDGING:

The arrow indicates when the balloon is inflated. There is a sustained increment in pressure reading.

img_1664

 

 

 

 

ACUTE MITRAL INSUFFICIENCY

Prominent v waves represent blood that enters the LA during ventricular systole due to an incompetent mitral valve.

img_1665

 

 

 

 

TRICUSPID REGURGITATION

Broad c-v waves can be seen.

img_1666

 

 

 

 

 

RV INFARCTION

Marked acute dilatation of the RV occurs. Acute dilatation is limited by the pericardium. Deep x and y descents, resembling the letter W is seen.

img_1667

 

 

 

 

 

MEASURED HEMODYNAMICS VARIABLES:

img_1648

DERIVED HEMODYNAMICS VARIABLES

img_1649

OXYGEN TRANSPORT VARIABLES

img_1650

Reference:

Criner, G., Barnette, R. and D’Alonzo, G. (2010). Critical Care Study Guide. Dordrecht: Springer.