Euglycemic DKA

Hi all. I wanted to bring to your attention a great case. The case was a young woman with relative euglycemic diabetic ketoacidosis. This diagnosis used to be quite rare and associated with pregnancy or very poor PO intake. However, with the use of SGLT2 inhibitors (which this young woman was taking) the incidence is increasing. The diagnosis highlights some very important factors about the treatment of DKA:

  • Don’t just look at the blood sugar. Calculate your anion gap. Look at the bicarb. Calculate the strong ion difference. Check for ketones. A VBG is fine for a rough estimate of pH. If you really want to get fancy, an ABG will give you an accurate base deficit that can help you figure out (along with your lactic acid, strong ion gap, or delta-delta) exactly what else is going on with the patient in the setting of multiple competing metabolic processes. But that’s only if you want to get fancy. I think you can provide great initial resuscitation without it.
  • Remember why we do what we do in DKA and all the complications you can get from treatment. The treatment is based on exactly the same principles that guide the treatment of “regular” DKA. However, they are not starting at the exact same metabolically disturbed place as most patients do. They can be just as sick, if not more, but the initial treatment has to take into consideration exactly where they are in their metabolic disarray. Things to think about as you are coming up with a treatment plan:
  • These patients need fluid. Fluid will be your friend (more on that later)
  • These patients need glucose. From the start. For a glucose less than 100-125, consider starting D10 instead of D5.
  • They need glucose because they need insulin too. They still may have some relative insulin resistance so giving them glucose alone won’t help them if they cannot get the glucose into any cells. However, as you are already starting from a lower glucose, be very gentle. If you still bolus insulin in DKA (which I do- in selected cases- and would be glad to have conversation about whether we should or not at another time) do NOT bolus these patients. I don’t have great evidence as to where to start a drip so I pick a low number. Like 1 low. I can always move up. If anyone has a better scientific explanation on how to pick your infusion rate, I’d love to hear it.
  • They need insulin so you better be sure you aren’t going to cause a malignant arrhythmia if you give it to them. Make sure your potassium isn’t going to plummet when you start insulin. Rough guideline is to make sure it is >3.3 . This is true for all DKA.
  • They don’t have a sodium correction because the glucose is normal. If their sodium is already on the higher side (around >140), think of starting with ½ NS as your base.

The attending on the case did an excellent job with this patient. He focused on fluid and recognized her severe metabolic disturbance, despite the fact that her blood sugar was trying to hide it.

I’ve included two articles below. One is two case reports on euglycemic DKA and the other talks specifically about cases involving SGLT2 inhibitors. They aren’t the best articles I’ve ever read but they are more official than I am so felt I should include them. As a said, this is a relatively new class of medications and a relatively new phenomenon.


Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma, EDM Case Reports, September 2017

Posted by:

Ruth Lamm, MD FACEP
Assistant Professor
Emergency Medicine
Critical Care Medicine
Saint Joseph’s Hospital Medical Center
lammr@sjhmc.org

Case of the week COW #10

CC: Nausea and vomiting and “ I think my sugar is low”

HPI: 36-year-old Female with PMH of Diabetes presents to the Emergency Department complaining of multiple episodes of non-bloody, non-bilious vomiting for the past 5 days. Associated symptoms include chills and a mild sore throat. Denies fever, HA, neck pain, chest pain, SOB, abdominal pain, diarrhea or bloody stools. Denies dysuria, hematuria or urinary frequency or urgency. Denies recent travels or sick contacts.   LMP: Currently menstruating

PMH: Diabetes

PSH: C-Section

Meds: None

Allergies: NKDA

Social: Admits to smoking 2 cigarettes per day for the past 10 years. Smokes marijuana daily. Denies alcohol use

 

Physical Exam : 

BP 171/82   HR 82    RR 20     SpO2 100% on RA    Temp 97.8F     108.86 kg

Constitutional: Alert, wake, and in no acute distress. Obese

HEENT: NCAT, pupils PERRLA, neck is supple. Oral mucosa is pink, dry and intact. No lesions. Normal conjuctiva

Respiratory: CTA B/L, no rales, rhonchi, no stridor or wheezing

Cardiac: +S1/S2, regular rate and rhythm, no murmur, rubs or gallop

Abdomen: Soft, with mild tenderness in epigastric area. No rebound or guarding. Normal BS

Neuro: AAO x 3. No focal deficits, moving all four extremities. Steady gate without difficulty.

MSK/Extremities: no edema, tenderness or swelling.

Skin: Moderate ecchymosis overlying RUQ and RUE. Normal moisture. No rash or lesions noted

 

Pertinent Labs:

WBC: 8.4   HGB: 9.3   HCT: 26.8   Platelet: 9L

Na: 136        K: 3.4          Cl: 104        Co2: 26      BUN: 16     Cr: 0.95   Glucose: 109

PT: 14.4   PTT: 28.7     INR: 1.1

Calcium 8.8         Total Bilirubin: 2.8       Alk Phos: 56           AST: 21                 ALT: 12

Lipase: 60

UCG: negative

Urinalysis: Large Blood with negative Nitrites and Leukocyte Esterase without ketones. UA Protein: 100

 Pertinent Images and other tests: Chest X ray: Borderline heart size. NO active disease

Upper Abdominal U/S: Normal Liver and spleen. The spleen measured 10.9 cm in greatest dimension and was homogeneous in echotexture. No focal splenic lesion identified. The liver measured 16.5 cm and appeared normal.

EKG:

 

Working Diagnosis:

Thrombotic Thrombocytopenia Purpura (TTP)

Idiopathic Thrombocytopenic Purpura (ITP)

Hemolytic Uremic Syndrome (HUS)

Anemia due to blood loss

Infection/Sepsis

ED Course: On further questioning, patient states she has been menstruating for 3 weeks now and bleeding is heavier as compared to the previous cycle. In the ED, patient was given NS 0.9% 1000mL IV bolus once, Zofran 4 mg IV once, Reglan 10mg IV once. Type and screen and blood cultures were also sent and patient was admitted to the Medical ICU for thrombocytopenia and anemia.

Hospital Course:

In the Medical ICU, further lab results demonstrated elevated the following:

LDH: 699         Fibrinogen: 410     Haptoglobin: < 10              Troponin 0.44

Blood Cultures: No Growth

Urine Toxicology: Positive for cannabinoids

Hepatitis C antibody: < 0.1

HIV Ag/Ab: Non reactive

In the ICU, patient was given a 125mg bolus of IV Solu-Medrol and then started on 60mg IV every 8 hours. She was transfused 1 Unit of platelet with no response, as the following day, platelets actually dropped to 5.Hematology/Oncology was also consulted. They stated that the occasional schistocytes seen on blood smear with low Haptoglobin levels and elevated reticulocyte count and LDH was suggestive of microangiopathic hemolytic anemia, making TTP a more likely diagnosis. Heme/Onc recommended against any further platelet transfusion and ADAMS 13 levels were sent. On hospital day #3, patient’s LDH levels had increased to 1586 and Troponin was elevated to 1.2 with symptoms of dyspnea. Patient also had worsening anemia as hemoglobin dropped to 7.0, and platelets remained at 9. The same day, Surgery was consulted and patient was transfused 2 Units of PRBs and 2 Units of FFP in preparation for Shiley Catheter insertion for plasmapheresis. Cardiology was also consulted for the elevated troponin, which they attributed to ongoing demand ischemia without any evidence of ACS. Unfortunately, the following night at 1:25 AM and before a Shiley was ever placed, the patient became minimally responsive and Saturating at 90% on RA. Immediately, she became bradycardic and lost pulses. CPR was initiated as patient was simultaneously intubated. Total duration of CPR was 60 minutes. The patient received Epinephrine x 20, Amiodarone 300 mg x 1 and Insulin with 1 amp of D50W, Calcium chloride and Sodium Bicarbonate for Potassium of 6.1 on ABG. Sadly, the patient was pronounced at 2:25AM.

PEARLS : Thrombotic Thrombocytopenic Purpura (TTP)

PENTAD = ‘FAT RN”

  1. Fever (50%)
    • Uncommon if they present early in the disease
    • High fever and chills suggest sepsis, so look for a source of infection.
  2. Thrombocytopenia
    • MAJOR diagnostic criterion
    • Mean platelet of 25, 000 but they reach 5000.
  3. Microangiopathic Hemolytic Anemia
    • MAJOR diagnostic criterion
    • Non-immune hemolysis with schistocytes
    • Results in elevated LDH, Low haptoglobin and high indirect bilirubin
    • Severely elevated LDH has been associated with MI, arrhythmias, shock and heart failure.
  4. Renal Failure
    • Due to renal thrombotic microangiopathy
    • Urinalysis will show mild proteinuria +/- hematuria
    • Acute Rena insufficiency may be present and may require dialysis.
  5. Neurological Symptoms: (Seizure, AMS, HA, coma, hemiplegia, aphasia, etc.)
    • Focal Deficits less prevalent
    • Occurs in 25-60% of patients
    • Symptoms are usually transient and subtle, so you must ask the patient about prior symptoms!

*** KEEP in mind; all features of the PENTAD do NOT to be present at the same time for diagnosis to be made.

Risk Factors

  • Obesity
  • African American race
  • Female
  • Ages 30-50 years
  • HIV/AIDS
  • Rheumatologic/autoimmune disease history

 Clinical Presentation

  • Fatigue, tachycardia, pallor, SOB or chest pain
  • Abdominal pain, back pain, Nausea, vomiting or diarrhea
  • New Onset jaundice and dark colored urine

Physical Exam

  • Diffuse, non-palpable petechial/purpuric rash.

Etiology

  • ADAMTS-13 protease enzyme deficiency
    • 60% of cases
    • Enzyme cleaves von Willebrand factor (vWF) multimers. Without it, excessive platelet aggregation, thrombocytopenia and thrombosis occurs
  • Idiopathic or Secondary Causes
    • 40% of cases
    • (i.e. HIV, malignancy, Infection, Pregnancy, pancreatitis, autoimmune disease, pancreatitis and medications such s Acyclovir, Quinine, Oxymorphoine, Plavix and Tacrolimus)
  • Diagnosis/Lab findings
    • NORMAL PT, PTT and Fibrinogen levels (Unlike in DIC)
    • Thrombocytopenia
    • Anemia and elevated indirect bilirubin
    • A peripheral smear is important for diagnosis, as 100% of patients will have schistocytes present during the course of the disease
    • ADAMTS-13 activity < 10% (normal activity is > 50%)

*** Remember that TTP is a clinical diagnosis. Do NOT delay treatment!

  • Differential Diagnosis
    • Other Causes of Microangiopathic Hemolytic Anemia (MAHA)
      • DIC, HUS, HELLP Syndrome, Malignant Hypertension, Heparin induced thrombocytopenia, Paroxysmal Nocturnal Hemoglobinuria, etc.
    • ITP
    • Sepsis
    • SLE
    • Viral infections (HIV, mumps, varicella, EBVS)
  • Management
    • Consult Hematology!
    • AVOID Platelet Transfusion if possible!
      • It can lead to renal failure, higher rates of arterial thrombosis and death
      • Should be AVOIDED EXCEPT in life-threatening bleeding or ICH
    • Plasma Exchange (Plasmapheresis) is First Line treatment!
      • Replaces defective or insufficient ADAMTS-13 and clears vWF multimers
      • LDH can be used to evaluate for treatment response
    • FFP Transfusion
      • Contains ADAMTS-13
      • Can be helpful if delay in plasmapheresis
    • Transfusion of RBCs (indicated ONLY in severe bleeding with a delay in plasma exchange)
    • Glucocorticoids
      • Adjunct Treatment and do not replace plasmapheresis
      • 1mg/kg Prednisone PO or Solu-Medrol 125mg IV
    • IVIG
      • Not first line but may be used in those who fail plasmapheresis
    •  Splenectomy
      • Last line therapy after stabilization
      • Inhibitor antibody is made in the spleen

Suspect TTP in any patient with MAHA and thrombocytopenia!

Case presented by Dr. Yenisleidy Paez Perez, DO

ACEP Now Review on LVADs

Check out this excellent review on managing patients with LVADs from this month’s ACEP Now publication which was written by our own Dr. Yenisleidy Paez Perez, DO PGY-3 and one of our newly graduated residents, Dr. Terrance McGovern, DO. The article is entitled ‘How to Manage Emergency Department Patients with Left Ventricular Assist Devices.” Click the link below to be forwarded to the article.

http://www.acepnow.com/article/manage-emergency-department-patients-left-ventricular-assist-devices/

EM Conference Pearls (8/2/17)

Pearl’s from Wed conference August 2nd 2017:

Agenda:
– Asthma/COPD: Baldino
– Sepsis Core Measures: Patel
– Pulmonary cases: Patel
– Medical student pearls (from Mike Taylor, one of our students)


Dr. Baldino: Asthma/COPD

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium,  and BiPAP.
-Intubation last resort for asthma.  Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD.  Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)


Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time.  To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost.  Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.


Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU.  If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.


Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
 -Can use a double lumen ET tube with a endobronchial cuff
 -The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
 Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Rate Control for MAT:

Take home points from Uptodate
 -Treat underlying cause
 -Maintain phos and mag levels
 -Can use CCBs or beta blockers for rate control in symptomatic pts
 Reference (requires access to UpToDate): https://www.uptodate.com/contents/multifocal-atrial-tachycardia

Bandemia Cut Offs:

Take home points from 2012 Retrospective Cohort Study:
 -With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
 -So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
 Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

Steroids for SJS and TEN?

Here’s a quick hit summary of the evidence regarding the use of systemic corticosteroids in the treatment of SJS/TEN

  • Small amount of evidence, NO RCT to date
  • Small retrospective study (n=30, groups comparable) in 1984 from a burn center found survival benefit (66% versus 33% survival) in NOT giving steroids. Also found decreased complications such as Candida sepsis & esophageal ulcer in patients who did NOT receive steroids.
  • Cohort of ~500 patients from RegiSCAR (International Registry of Severe Cutaneous Adverse Reactions to Drugs)
    • No statistical diff in Hazard Ratio among treatment groups (supportive care vs. corticosteroids vs. IVIG).
  • Systematic Review of literature from 2001-2009 (only used Pubmed, not great)
    • Pooled analysis demonstrated no statistically significant difference in Mortality Ratio among groups (supportive care vs. corticosteroids vs. IVIG).
    • B.: i2 statistic not reported but authors mention no problematic heterogeneity.
  • Very small study (n=12 over 10 years) demonstrated potential benefit to early pulse-dose IV steroids (1.5 mg/kg/day dexamethasone for 3 days) in the form of (1) disease halt at 3 days (2) 1 actual death versus 4 predicted deaths.
  • Interestingly, a case-control study (case n=92; control n=381) demonstrated that pre-existing chronic steroid use delayed onset of SJS/TEN in patients using high-risk drugs by 7 days but also prolonged disease course by 2 days.

Bottom line

  • Systemic corticosteroids have not been shown to consistently correlate or provide a survival benefit in patients with SJS/TEN.
  • Paucity of evidence may show benefit to pulse-dose IV steroids such as are used in the treatment of autoimmune diseases such as pemphigus vulgaris.
  • Supportive care is the standard of care.

Post by: Dr. Katrina D’Amore DO, MPH

Case of the Week #3 – Why my flap sunken?

CC: Altered mental status and frequent falls

HPI: 55 y/o male presents from rehab with altered mental status (lethargy and agitation) and frequent falls for the past 2 days. Patient has a PMHx of large traumatic subdural hematoma 9 months ago treated with a craniectomy, seizure disorder, and HTN. Patient complains of headache and is a difficult historian. Pt does answer some questions appropriately.

Pertinent PE and Vitals: BP 121/81 HR 98 RR 16 Temp 98.1 100% on RA

GCS=14 and in no acute distress

L pupil dilated at 4 mm and nonreactive. R pupil 1 mm and reactive.

Pt. with moderate R arm and leg weakness (patient has baseline weakness but this is worse).

Pertinent Labs (if any): Unremarkable workup

Imaging

Working Diagnosis at time of Disposition Sinking Skin Flap Syndrome (also known as Syndrome of the Trephined) with possible Paradoxical Herniation

ED & Hospital Course Patient was admitted and received neurology and neurosurgical consultations. Medications were adjusted to control agitation. It is questionable per the consultants if his symptoms were due to paradoxical brain herniation. Plan is for an outpatient cranioplasty.

Pearls & Takeaways

  • Sinking skin flap syndrome is a delayed complication of a decompressive craniectomy. As the herniated brain tissue recedes, the skin flap from the surgical site can become sunken.
  • Symptoms include headaches, dizziness, seizure, and mood changes.
  •  Symptoms worsen when is head elevated vs reclined; treatment option is cranioplasty. Symptoms are much worse in an upright posture.
  • If atmospheric pressure exceeds intracranial pressure, patients can get paradoxical herniation and midline shift. This is more of an emergency and symptoms include focal deficits, pupillary changes, and alterations in consciousness.
  •  Paradoxical herniation is a state of low intracranial pressures; therefore traditional measures to treat midline shift and ICP will worsen the condition such as mannitol, hyperventilation, etc.
  • Treatment of sunken skin flap with paradoxical herniation is to elevate the intracranial pressure, including Trendelenburg position, hydration, and clamping of any CSF drains. Definitive treatment is cranioplasty.

Antibiotics for chest tubes

Things to keep in mind:

Prophylactic antibiotics for surgical patients in tube thoracostomy is usually limited to 24hrs duration and is 1st generation cephalosporin. It is meant to cover s. aureus the most common organism found in post traumatic empyema

increasing antibiotic use is leading to increase incidence of drug resistance

Potential infectious complications of penetrating or blunt chest trauma:

  • Post Traumatic Empyema
  • Pneumonia

Literature is mixed on whether antibiotics should be given for chest tubes placed for trauma.

In 1998 EAST guidelines gave a level 3* recommendation to give antibiotics prophylacticly to reduce incidence of pneumonia based off of Class I and Class II** data. AND there was insufficient data to give prophylactic antibiotics for post traumatic empyema

This recommendation remains controversial because 

  •    In order for antibiotics to be prophylactic they have to be given prior to a procedure and must reach a steady state concentration in the tissue before an incision is made.
  •    In the case of antibiotics given after a trauma has already occurred, the pleura has already been violated regardless of whether it is penetrating or blunt trauma. Therefore antibiotics do not reach needed concentration before contamination has concerned so these antibiotics are considered presumptive antibiotics.
  •    Non standard definitions of pneumonia and empyema were used, as well as various antibiotics were used in the different studies

In 2012 EAST guidelines reviewed the use of presumptive antibiotics for chest tubes (Tube thoracostomy):

They decided that they cannot make a recommendation for or against the routine use of presumptive antibiotics for chest tubes placed for traumatic hemopneumothorax.

Nor are they able to recommend an optimal duration of antibiotic prophylaxis when antibiotics are administered for traumatic hemopneumothorax because there are insufficient published data to support the routine use of antibiotics.

They concluded:

No single published study has been powered to adequately address the practice of administering presumptive antibiotics in TT for traumatic hemopneumothorax to decrease the incidence of empyema or pneumonia. Until a large and likely multicenter, randomized, controlled trial can be performed, the routine practice of presumptive antibiotics in TT for chest trauma will remain controversial.

If you want to read the article it isn’t a long read:
Post by: Dr. Ashley Guthrie, DO

Case of the Week #1

CC Chest pain and palpitations

HPI Pt is a 23 y/o male with no PMHx presenting with c/o palpitations, chest pain since last night. Pt states the pain is localized to the mid sternal chest wall with radiation to b/l upper extremities at times. Pt states the pain came on suddenly last night and he didn’t think anything of it so he went to bed. He woke up this morning with same pain and now with associated nausea and dizziness prompting the visit to the ED. Pt has never had pain like this in the past. Denies vomiting, F/C, recent illness, sudden cardiac death in the family other than a 70 y/o uncle who was obese. Pt denies drug use and states he was drinking over the weekend 2 days ago.

PMHx: none

Meds: none

Allergies: none

PSHx: none

Social: occasional ETOH, (-) drugs

Pertinent PE and Vitals: BP 90/62 P 186 RR 22 O2 sat 100% RA

General: Awake, alert, mild distress Cardiac: (+) tachycardic; no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, nontender, nondistended Skin: diaphoretic; mild pallor

Pertinent Labs (if any) Troponin: 0.439

DDX: SVT with aberrancy vs VTach

ED Course: Pt placed on cardiac monitor immediately and IVF bolus initiated. Adenosine 12 mg IVP given while rhythm strip running with no change. A second dose of Adenosine 12 mg IVP given again with no change. 150 mg Amiodarone given with improvement of HR from 190’s to 170’s still wide complex. Second dose of 150 mg Amiodarone given with improvement of HR from 170‘s to 150’s and eventually converted to a NSR rate 85. Pt remained in stable condition and BP responsive to IVF. Pt admitted to telemetry and Cardiology consulted. While still in the ED, pt reverted back to wide complex tachycardia. 3rd dose of 150 mg Amiodarone given and recommendation from Cardiology was to try a 20 mg IVP of Cardizem. Cardizem given and pt immediately converted to NSR. Pt started on Cardizem drip and upgraded to the CCU. Pt underwent EPS and AV dissociation was noted. Determination was Verapamil Sensitive Ventricular Tachycardia. Pt remained stable throughout hospital course and started on Verapamil. Discharged on hospital day #3 with follow up with cardiology clinic.

Final Dx:  Idiopathic Fascicular Left Ventricular Tachycardia AKA • Fascicular Tachycardia • Verapamil-sensitive VT • Belhassen-type VT

Discussion:  MC type of idiopathic tachycardia of LEFT ventricle ! It is a reentrant tachycardia typically seen in young patients without structural heart disease ! Verapamil is first line treatment • Dose: 10 mg IVP over 1 minute ! EKG features: • Monomorphic V tach • QRS 100-140 ms (narrower than other forms of Tach) • Short RS interval 60-80 ms • RBBB pattern • Axis deviation depends on anatomical site of re-entry circuit ! Often misdiagnosed as SVT with RBBB ! Keys to dx: • Observe features of VT such as caption/fusion beats, AV dissociation • Usually unresponsive to adenosine, vagal maneuvers, or beta blockers

Post by: Kristen Pena, DO

Getting ready to intubate? Let’s pray they don’t DESATurate!

You head over to bed 44 to meet the BLS crew as they start telling you about an 82 year old man who has been having trouble breathing and is “confused” as per his family.  His oxygen saturation when you check is 76% and quicker than you can say “sepsis”, the eager resident has popped the grey airway box open and is setting up to intubate.

You slap the NRB on and turn the O2 up all the way.  So why is the resident so focused on finding and placing a nasal cannula too?!

Apneic oxygenation (AO) is used to extend the time until critical arterial desaturation (SaO2 88-90%) following cessation of breathing/ventilation that occurs during intubation.  AO, similar to our other RSI preparation, premedication, and positioning, is used to optimize the patient prior to the first intubation attempt.

First demonstrated by anesthesiologists over 50 years ago, the alveoli of the lungs will continue to take up oxygen even in the absence of active breathing.  AO focuses on increasing a patient’s oxygen saturation through “nitrogen washout” in first the alveoli, and then throughout the circulation.  This effectively replaces the nitrogen one inhales in normal atmospheric air with oxygen and increases the patient’s overall oxygen storage in both the lungs (95% of a person’s natural reservoir) and bloodstream.  Maximizing pre-oxygenation provides us an additional buffer of time for “safe apnea” during oral intubation.  In a 2011 article in the Annals of Emergency Medicine, Weingart et al outline recommendations to reduce the risk of hypoxemia during emergency tracheal intubations which include emphasis on:

Pre-oxygenation for every patient

  • Nasal Cannula set at 15 L/min is the most effective method of AO
  • Non-rebreather mask at rates as high as possible
  • HOB elevated 20-30 degrees or Reverse Trendelenburg in suspected C-spine injuries
  • Minimum of 3 minutes total or 8 deep breaths, if possible

Take home:  Keep in mind the acronym “NO DESAT” which stands for “Nasal Oxygen During Efforts Securing A Tube”.  A nasal cannula with high flow rates should be placed on every patient prior to endotracheal intubation and left in place during attempts in order to reduce the risk of hypoxemia and deterioration.

TLC: Triple Lumen Complications

Placing central venous cathethers, whether under ultrasound guidance or based off of your landmarks can be difficult and still prone to many complications.  With the increased use and now standard of care for placing central lines with ultrasound guidance you would think we are immune to the “catastrophic” complication of an inadvertent arterial cannulation.  But does ultrasound make us infalliable? Are there other methods that we can use to confirm venous placement of these large catheters?

Traditionally, we have looked at the color and pulsatility of blood coming from the needle hub before placement of the guidewire, but as you can imagine this is known to not be the most reliable; most of us aren’t going to go through the hassle of checking a blood gas off that blood either.

Troianos et al. found that ultrasound guidance reduced the incidence of arterial puncture from 8.4% down to 1.4% during attempted IJV cannulation.  That’s great that it decreased the incidence, but when looking at the complications such as airway obstruction, hemothorax, pseudoaneurysms, AV fistulas and stroke, 1.4% is not something to sneeze at.  So, keep in mind that although it does reduce the frequency of arterial puncture, it does not eliminate it entirely!

Despite the use of dynamic ultrasound guidance, there are still numerous reports of arterial placement of large bore catheters due to a couple reasons: 1. The needle tip may not be seen in the same plane of the ultrasound and confused with the shaft of the needle.  2. The needle may be in the vein, but the needle may move into the artery during placement of the guidewire after most of us have abandoned the ultrasound visualization.  Ideally, after the guidewire is placed we should make it a habit to confirm the guidewire is in the vein before dilating the vessel.

Management of Arterial Cannulation

Despite our best efforts and even the most astute ultrasonographer there is always the potential for an inadvertent arterial cannulation, but what do we do once we have figured that out?

Option 1: Just old fashioned PULL AND PRESSURE: essentially this is exactly as it sounds. You pull out the catheter and apply pressure, just like any other line that is being removed. This is probably most reasonable for femoral artery cannulations, but there still remains a possibility of false aneurysms and AVF as late as 2 weeks after removal with the pull and pressure technique.  Pull and pressure isn’t supposed to be used for carotid or subclavian arterial cannulations.  One convincing piece of evidence is that there is an immediate stroke risk of 5.6% after removing carotid cannulations with this technique.  Of 11,874 internal jugular vein cannulations, 20 ended up being carotid artery cannulations.  19 of these 20 were removed using the pull and pressure technique; six patients suffered complications and two of the patients died.

Option 2: Surgical ENDOVASCULAR repair:  The more preferable method, especially for removal of carotid and subclavian arterial cannulations, is to involve our vascular surgeon colleagues.  Just leave the line secured to the neck and get them involved. Some are going to request a formal ultrasound of the carotid or even sometimes a CT angio of the neck to check for extravasation, pseudoaneurysms, AVF and the location of the catheter.

Key points to remember

  1. Arterial cannulation can occur despite use of ultrasound guidance
  2. The American Society of Anesthesiologit’s guideline for CVC placement states that color and pulsatility are NOT reliable for distinguishing vein from artery.
  3. The pull/pressure technique is associated with significant risk of hematoma, airway obstruction, stroke, and false aneurysm especially when the site of arterial trauma cannot be effectively compressed
  4. Low IJV placement can injure the subclavian or innominate arteries
  5. Endovascular treatment is safe for management of arterial injuries that are difficult to expose surgically, such as those below or behind the clavicle.
  6. Normal Carotid Duplex after removal of a catheter form carotid artery does NOT rule out the possibility of a stroke
  7. False aneurysms or AV fistulae can occur LATE, up to 2 weeks after the “pull and pressure” technique so close follow up is needed

Post by: Dr. Yenis Paez-Perez, DO