After hours discharge, increased mortality

Hot off the online press is this article, the authors of which include our own Dash Gantner and David Pilcher:

Gantner D et al. Mortality related to after-hours discharge from intensive care in Australia and New Zealand, 2005–2012. Intensive Care Medicine, [Accessed 18 August 2015 at URL: http://icmjournal.esicm.org/journals/abstract.html?v=0&j=134&i=0&a=3438_10.1007_s00134-014-3438-x&doi=]

This study shows that the proportion of patients discharged after-hours from ICUs around ANZ hasn’t changed in 8 years, and nor has the associated risk of mortality. These findings are disappointing because concerns about the risks of after-hours discharge have been held for years, yet we seem to have had little success in addressing them.

Here is the study at a glance:

  • It is the largest-ever study of ICU discharge timing – over 700,000 admissions in Australasia from 2005-2012, with data extracted from ANZICS Adult Patient Database (APD)
  • 15.4% of patients were discharged after-hours (1800–0600 hours) overall, ranging between 14.8 to 15.9% depending on the year.
  • The overall odds ratio for mortality was 1.34 (range 1.32 – 1.37) when compared with in-hours discharges, after adjustment for illness severity and treatment limitations.

Unfortunately, this problem has not gone away – there is more work to be done!

To learn more read the Monash University media release: ICU fatalities linked to after-hours discharge.

Abstract

Introduction

After-hours discharge from the intensive care unit (ICU) is associated with adverse patient outcomes including increased ICU readmissions and mortality. Since Australian and New Zealand data were last published, overall ICU patient mortality has decreased; however it is unknown whether changes in discharge practices have contributed to these improved outcomes. Our aim was to examine trends over time in discharge timing and the contemporary associations with mortality and ICU readmission.

Methods

Retrospective cohort study using data from the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS APD) for patients admitted to Australian and New Zealand ICUs between January 2005 and December 2012. Data collected included patient characteristics, time of ICU discharge, hospital mortality and ICU readmissions.

Results

Between 1 January 2005 and 31 December 2012, there were 710,535 patients available for analysis, of whom 109,384 (15.4 %) were discharged after-hours (1800–0600 hours). There were no changes in timing of ICU discharge over the 8 years of the study. Patients discharged after-hours had a higher hospital mortality (6.4 versus 3.6 %; P < 0.001) and more ICU readmissions (5.1 versus 4.5 %; P < 0.001) than patients discharged in-hours. Although post-ICU mortality for all patients declined during the study period, the risk associated with after-hours discharge remained elevated throughout (odds ratio 1.34, 95 % confidence intervals 1.30–1.38).

Conclusions

After-hours discharge remains an important independent predictor of hospital mortality and readmission to ICU. Despite widespread dissemination this evidence has not translated into fewer after-hours discharges or reduction in risk in Australian and New Zealand hospitals.

The post After hours discharge, increased mortality appeared first on INTENSIVE.

What Causes Proteinuria?

Patient Presentation
A 16-year-old female came to clinic because of 2 days of dysuria. She was having some increased frequency and also pain with urination. She wasn’t sure if the pain began with the bladder contracting or when her urine stream touched her genital area. She denied fever, chills, nausea, emesis, constipation or pain with defecation. She also denied previous bladder infections or sexual activity. The family history was negative for renal disease or hearing problems. The social history showed her to be a cross-country runner who had increased her mileage the past week by almost 50%. The review of systems was negative.

The pertinent physical exam showed a healthy female with no distress. Her blood pressure was 106/62, pulse of 68 and respiratory rate of 16. She was afebrile and her growth parameters showed a weight of 25%, and height of 75%, consistent with previous measurements. Her abdomen examination was negative including no suprapubic or costovertebral angle tenderness. Genitourinary examination revealed diffuse erythema of the vaginal area and perineum.

The diagnosis of skin irritation due to contact with sweat and clothing friction was made. The patient was advised to change into clean clothing often, not tuck her shirt into her pants to help keep moisture away from the genital area and to use sports lubrication products to decrease the friction from her clothing. Because a bladder infection could not be fully ruled-out a laboratory evaluation of a urine dip was done and showed a specific gravity of 1.015, 2+ protein and negative leukocyte esterase and blood. Because of the protein, the physician reviewed her chart more closely and saw normal blood pressure readings and also a BUN and creatinine that were normal during an emergency room visit for head trauma The physician thought that the proteinuria was most likely due to the increase in exercise. The patient’s clinical course over the next few weeks found none to 1+ protein in the urine, and which resolved after the cross-country season finished.

Discussion
Proteinuria occurs relatively often in pediatric practice with 5-15% of school children having transient proteinuria, the most common cause. However, proteinuria can be a sign of kidney disease. Therefore, it is important to evaluate the proteinuria in light of the clinical situation. A good history and physical examination along with a full urinalysis and/or BUN and creatinine, or urine protein/creatinine ratio may be all that is necessary. Another patient with edema, hypertension or hematuria needs a fuller evaluation and treatment. Proteinuria is usually categorized into three groups to assist with evaluation and treatment and they include: transient, orthostatic or persistent.

Transient means just that. It occurs only during the inciting problem and remits afterwards. It generally is < 2+ on a dipstick. Proteinuria due to fevers usually resolves in 10-14 days, and exercise induced proteinuria remits within 48 hours of the exercise.

Orthostatic (postural) proteinuria is proteinuria that occurs in the upright position only. It can be intermittent or persistent. It is the most common cause of asymptomatic proteinuria in children especially adolescents. Protein excretion in the recumbent position is < 4 mg/m2/hr and in the upright or ambulatory position is 2-4 times this amount.

Persistent asymptomatic isolated proteinuria occurs in children and laboratory and clinical testing is otherwise normal. The protein is monitored every 6-12 months and if protein is rising then renal biopsy may be indicated. Glomerular diseases all have proteinuria. One of the most common in children is nephrotic syndrome due to minimal change disease. Nephrotic syndrome has the following characteristics: proteinuria, hypoalbuminemia, hypercholesterolemia and edema.

An urine dipstick is often used to interpret proteinuria. The amounts of protein are shown here:

Trace = 10-20 mg/dL
1+ = 30 mg/dL
2+ = 100 mg/dL
3+ = 300 mg/dL
4+ = 1000-2000 mg/dL

“A urine sample is positive for protein if the dipstick is [> or =] 1+ on a urine sample with a specific gravity of [ 1.015, the dipstick must be [> or =] 2+ to be considered positive.”

Learning Point
The differential diagnosis of proteinuria includes:

  • Transient proteinuria
    • Cold exposure
    • Congestive heart failure
    • Epinephrine administration
    • Exercise
    • Fever
    • Seizures
    • Serum sickness
  • Orthostatic
  • Persistent asymptomatic isolated proteinuria
    • Glomerular disease
      • Nephrotic syndrome, minimal change
      • Alport syndrome
      • Glomerulonephritis
        • Membranoproliferative
        • Post-infectious
      • Henoch-Schonlein purpura
      • HIV-associated nephropathy
      • IgA nephropathy
      • Sickle cell anemia
      • Systemic lupus erythematosus, nephritis
      • Vasculitis
    • Tubulointerstitial disease
      • Fanconi anemia
        • Dent’s disease
      • Interstitial nephritis
      • Ischemia
      • Reflux nephropathy
      • Renal dys- or hypoplasia
      • Medications
        • Aminoglycosides
        • Lithium
        • Penicillin

Questions for Further Discussion
1. What are indications for renal biopsy with proteinuria?
2. What are causes of falsely-positive proteinuria on dipstick?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Urine and Urination and Kidney Diseases.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Ariceta G. Clinical practice: Proteinuria. Eur J Pediatr. 2011 Jan;170(1):15-20.

Hladunewich MA, Schaefer F. Proteinuria in special populations: pregnant women and children. Adv Chronic Kidney Dis. 2011 Jul;18(4):267-72.

Kaplan BS, Pradhan M. Urinalysis interpretation for pediatricians. Pediatr Ann. 2013 Mar;42(3):45-51.

ACGME Competencies Highlighted by Case

  • Patient Care
    1. When interacting with patients and their families, the health care professional communicates effectively and demonstrates caring and respectful behaviors.
    2. Essential and accurate information about the patients’ is gathered.
    3. Informed decisions about diagnostic and therapeutic interventions based on patient information and preferences, up-to-date scientific evidence, and clinical judgment is made.
    4. Patient management plans are developed and carried out.
    5. Patients and their families are counseled and educated.
    7. All medical and invasive procedures considered essential for the area of practice are competently performed.
    8. Health care services aimed at preventing health problems or maintaining health are provided.

  • Medical Knowledge
    10. An investigatory and analytic thinking approach to the clinical situation is demonstrated.
    11. Basic and clinically supportive sciences appropriate to their discipline are known and applied.

  • Practice Based Learning and Improvement
    13. Information about other populations of patients, especially the larger population from which this patient is drawn, is obtained and used.

  • Systems Based Practice
    24. Cost-effective health care and resource allocation that does not compromise quality of care is practiced.

    Author

    Donna M. D’Alessandro, MD
    Professor of Pediatrics, University of Iowa Children’s Hospital

  • Tox Tunes #85: Goodnight, Irene (Jerry Lee Lewis and Van Morrison)

    http://www.youtube.com/watch?v=wmvCAzLseu8

    Goodnight, Irene” was introduced by the folksinger and blues musician Lead Belly (Huddie Ledbetter, 1888-1949) and became a big hit for The Weavers in 1950. This fascinating song tells a somewhat murky story about unrequited passion and suicidal fantasies. The Weavers, however, left out the reference to opiates in Lead Belly’s original lyrics:

    I love Irene
    I swear I do
    I love her ’til the sea runs dry
    If Irene turns her back on me
    I’m gonna take morphine and die.

    Jerry Lee Lewis and Van Morrison keep this verse in their version.

    Lead Belly’s original also implies love for a girl who is possibly underage, and also — at least to my interpretation — hints of murder. It limns a story that is much more coherent:

    http://www.youtube.com/watch?v=dRHHhObYMKE

    And here is The Weavers’ hit version from 1950. It is a much tamer, much less dangerous song. And I’ve never forgiven them for those awful strings:

    http://www.youtube.com/watch?v=s5aixNi_C1Q

     

    Trauma: Lessons from the Military. Wing Commander Dr Paul Nealis


     

     

    Key points

    Stop bleeding!

    Tourniquets are great.

    Pack bleeding wounds firmly.  A roll of gauze works well. “Haemostatic dressings” eg quik clot, don’t seem to make much difference.  It appears the pack needs to be absorbent probably because they absorb water out of the blood in the wound thereby increasing the concentration of clotting factors.http://emtutorials.com/wp-admin/post-new.php

    Don’t get hung up on big IV lines.  The difference in flow rate between a 18 and 16 gauge is not that great.  If the patient is bleeding out that fast they aint going to make it, and sometimes 18s are just easier to get in especially in a shocked patient.

    Permissive hypotension: aim for a systolic of 80 (90 if head injury).  Don’t rely on mental status (BP 60 systolic but compensating and still conscious… 60 and compensating  still conscious …. 60 and still conscious … dead).

    For massive haemorrhage transfuse and give tranexamic acid early.  For us this may mean sending an “unknown patient” label down to get some O-negative blood from the lab before the patient arrives.  Get FFP thawing ASAP. Get platelets ASAP.

    Use ketamine rather than fentanyl in major trauma -> lives saved,  presumably by avoiding the sympatholytic effects of fentanyl

    Ketamine appears to reduce the incidence of Post Traumatic Stress Disorder by 60%!  This may be by reducing the patients’ experience of pain and mutilation.

    ED teams (in the military ED docs and nurses and military medics) resuscitate the patient, others behind the red line.  When the external bleeding has been stopped and the patient resuscitated, then the anaesthetist and surgeon are invited to take the patient to theatre/operating room

    Some of the slides:

    Audio only:

    The post Trauma: Lessons from the Military. Wing Commander Dr Paul Nealis appeared first on EM Tutorials.

    Amyl Nitrite Overdose: Clinical Case and Pearls

    The screen adaptation of S. Thompson's novel, Fear and loathing in Las Vegas, depicts the characters Raoul Duke and Dr. Gonzo using Amyl Nitrite in multiple scenes throughout the movie. 

    The screen adaptation of S. Thompson's novel, Fear and loathing in Las Vegas, depicts the characters Raoul Duke and Dr. Gonzo using Amyl Nitrite in multiple scenes throughout the movie. 


    This case and pearls are provided by Dr. Andrew Ketterer. Thank you so much for the excellent case! Edited by Michael Macias. 


    The Case 

    An adult male was wheeled into the emergency department appearing ashen gray with blue highlights. Knowing that this was not common in the expected human color palette there was significant immediate concern. Upon discussion with the patient, he frankly admitted to drinking 2 bottles of amyl nitrite in order to attempt to get high.

    The patient was alert and conversational, albeit disorganized. Almost immediately after getting shifted onto a bed he began to vomit copiously, filling the room with a tinny miasma of amyl nitrite. At this point our path was pretty well set: we got the airway stuff set up and our pharmacists dug out some methylene blue.


    Amyl Nitrite

    Before we get into lab values and treatment for the patient, let's discuss what amyl nitrite is and what we should be concerned about.

    Amyl nitrite is part of the alkyl nitrite family and has been used previously in medicine for its vasodilator properties given that it can act as a source of nitric oxide. However it also carries with it psychoactive properties which have led to its recreational use and high abuse potential. Typical positive sensations of amyl nitrite ingestion (usually via inhalation) include excitement and euphoria.  You can mix it into your cocaine to add on an extra duration of your high or increase tactile sensation. It can also be snorted on its own to act as an aphrodisiac (known, apparently, as “poppers”). Other less pleasant physical effects include headache, flushing, tachycardia, a warming sensation, relaxation of involuntary muscle and dizziness.

    More concerning, amyl nitrite is one of a list of drugs that cause oxidative stress on red blood cells: among other things, large amounts of this stuff can cause the oxidation of Fe2+ (normal hemoglobin) to Fe3+ (methemoglobin). Methemoglobin shifts the oxygen desaturation curve to the left, meaning that O2 has a harder time dissociating to get to the tissues leading to poor tissue perfusion. Hence in our case the ashen appearance of the gentleman's skin. 


    Case update

    The patient in our case had a pre-treatment methemoglobin level of 61%. For reference, physiologic levels of MetHb usually hover around 1-2%, and 70% is generally regarded as being incompatible with life.

    Fortunately, despite a pulse ox reading of 84% (actual PaO2 155 mmHg), the patient maintained his mental status and we weren’t forced to tube him. Approximately 30 minutes after receiving one weight based dose of methylene blue he began to pink back up and he became a little more coherently conversant. His repeat MetHb had improved to a level of 9%.


    Some pearls

    • Sodium nitrite which is in the similar family as amyl nitrite is sometimes used as an antidote for cyanide poisoning (generates methemoglobin which then binds cyanide) though hydroxocobalamin has now become the preferred treatment. 
    • Don't believe your pulse oximeter: The probe functions by using 2 wavelengths of light (red and infrared) to measure the ratio between oxyhemoglobin and deoxyhemoglobin. MetHb absorbs equally at the red and infrared wavelengths used by traditional pulse oximetry, which results in an erroneous SpO2 readout near 85%. Our patient’s actual arterial O2 content was 155 on non-rebreather face mask.
    • Give methylene blue, but don’t overdo it. Methylene blue donates electrons to the NADPH pathway (a minor one for reducing Fe3+ to Fe2+), and allows conversion of methemoglobin back to hemoglobin. However, methylene blue itself can cause methemoglobinemia when given in excess, and if the person also takes SSRIs, SNRIs, or MAOIs it can precipitate serotonin syndrome by reversibly inhibiting monoamine oxidase A. The Illinois Poison Control Center recommends a single dose of methylene blue at 1-2mg/kg over 5 minutes to treat methemoglobinemia. In severe cases such as this one, more than one dose may be required, but this hinges primarily on clinical status (mental status and airway protection), as well as continued resolution of the methemoglobinemia.
    • Make sure to cover your other tox bases. Be sure to be on the lookout for a co-ingestion. In addition to checking MetHb levels every 2 hours, we checked COHb, acetaminophen, salicylate, and alcohol levels. Urine tox screen may help if it would possibly alter your management. We also obtained a liver function panel and coagulation panel (the reason for the latter being that if the person has chronic liver damage the only way you might see an acute change is by new coagulopathy). The reason for all this is that you want to cover all your potentially reversible bases in toxicologic emergencies; it’d be bad news if we treated this guy’s methemoglobinemia only to find out later that he’d also taken a couple bottles of Tylenol and blasted out his liver.

    Closure

    As it was, this guy improved a lot and was sent up to the MICU for monitoring. He was also extremely pleasant throughout the whole thing, which given how close to death he was is pretty impressive.


    References

    Faley B and Chase H. “A Case of Severe Amyl Nitrite Induced Methomoglobinemia Managed with Methylene Blue.” J Clin Tox. 2012, 2:4.

    Cortazzo J and Lichtman A. “Methemoglobinemia: A review and recommendations for management.” J Card Vasc Anes. August 2014. 28(4): 1055-1059.

    Original photo from picture provided by: http://pitch.rs/3-copywriting-mistakes-that-are-driving-your-customers-away/fear-and-loathing-in-las-vegas-fear-and-loathing-in-las-vegas-12935663-1920-1080-2/