Volume 04:

Episodes 076 - present

Patient - young man brought in by EMS CPR in progress (during COVID). PEA on monitor – no vitals. Appeared pale and cyanotic – EMS had a suicide note and a bottle of sodium nitrate from the patient's residence.

Staff were able to contact a colleague who was a toxicologist specialist for advice. It took an extended period to get poison control on the phone. The patient was intubated, and multiple lines started.

Recommended starting Methylene blue started (color of blue ink) started running right away and continued with CPR. The patient started turning blue as infusion began circulating. Redosed q 5 min (5-6 doses total) – after 45 min of CPR patient remained in PEA and time of death was called.

Concerns for how the patient was able to obtain it and suspect possible online purchase? Unknown how patient was able to obtain sodium nitrate

☙ Sodium Nitrate (nitrates) causes methemoglobinemia. The Fe2+ (healthy) atom in hemoglobin is oxidized to Fe3+ rendering the molecule unable to carry oxygen efficiently. Methemoglobinemia turns RBCs a chocolatey brown colour but seen through the skin, appears as a profound cyanosis
☙ Methylene Blue treats methemoglobinemia by reducing the Fe ion back to 2+. Thus despite being a richly blue colour itself, it actually helps to resolve cyanosis in this context.


080 - How to become a better Rural Resuscitationist  

What is Resuscitation – making clinical decisions based on limited time and information – gambling essentially.

The sicker and more unstable they become, the greater their risk.
Be comfortable with making important decisions with limited information and accepting the risks you may make the wrong decision and that sometimes there is harmful outcomes
       - Know that failure to act and decide is also a choice and has its own consequences.

Be aggressive when resuscitating – especially pre-arrest patients
       - Delay in treatment and loss of pulse results in damage control and trying to recover with minimal brain damage if possible.
       - There are no black-and-white recommendations in pre-arrest patients
       - there is a risk of having underlying causes that lead to death based on the treatment given.
       - Identifying anything time-sensitive - don’t delay
Ex:
☙ Anaphylaxis or sepsis – once identified or high suspicion – treat!
☙ Toxicology – treat with activated charcoal if possible
☙ Toxic shock – remove (replace if needed with clean dressing), use caution with abx in this case.
☙ Critical Bradycardia – give atropine.
☙ Critical hypotension – start a vasopressor (whatever you have or are comfortable with to start) to stabilize and switch to a different pressor afterwards if needed
☙ Look at H’s and T’s for initial diagnosis and treat quickly in ACLS

Slower decline patients in delirium
       - Small dose of ketamine to help sedate 
Phoning a friend – causes delays of min 5 and greater – attribute the harm that comes with delays.

Protocols of resuscitation
IV fluid – 2 L of fluid – much time spent on what fluid to give and how fast to run it in – Don’t delay other treatments on fluid. Other times, there are other more effective treatments than just fluid.

☙ Think ahead to be ahead – while waiting for transport, think about what is coming next – transport. Try to be two steps ahead of where the patient is at. What might the patient need next – set up for airway, set up for vasopressors and pump programmed ready to go, get d-fib pads on if cardiac issues arise (ex. STEMI or arrhythmia patients)

☙ Think about barriers to transport!
       - What can you do to expedite the process? Team arrival is not the saviour.
       - It’s the destination the patient is going to.
       - The goal is to help the transport team as much as possible.
       - Delaying basic interventions can be detrimental to patient care and delay transport to definitive care.
Ex. What drugs are the patient going to need and get them going prior to transport? If you can give them meds before transport and reduce the amount needed in transport, that would be better.
       - If IV is not reliable, then start another. Consider a central line or IO.
       - Heavier sedation during transport is normal due to the amount of stimulation experienced during transport.

Resuscitation is rarely black and white where you know 100% what to do. Get comfortable with having a limited picture and play the odds and probability of the patient's best interests.

☙ Analysis Paralysis is how you lose at the resuscitation game.
☙ Get comfortable with being uncomfortable


Case

55yo male previously diagnosed with major depressive disorder (MDD) being treated with fluoxetine and going through marital problems with worsening mood.
       - Took 10 -15 tablets immediate release Asprin 325mg – no co-ingestion

Time to assessment is 2 hours post-ingestion and feeling at baseline during the exam. Vitals normal. Physical exam normal. No activated charcoal was given due to the time elapsed.

☙ Toxic ASA levels 150mg/kg – pt toxic dose is 12,000mg. Pts reported dose is 3000mg based on the 10-15 tablets reported.

Patients Serum level - 3.65mmol/L reported back from the lab – Critical value.

☙ Management
       - If no toxicological level is available but the patient is presenting with s/s of:
              - OD (ex., tinnitus, hyperventilation, vomiting, seizures, respiratory distress, hyperthermia), these are good clinical clues.
       - ASA level of greater than 3.5mmol/L
       - Presence of metabolic acidosis

***Endpoints of therapy (3 points that all have to be met)***
       - ASA level of less than 2.2mmol/L
       - Two consecutive ASA levels of declining trend
       - Clinically patient must be doing well

ASA OD – thinking ahead
       - If you think it is serious – start arranging for dialysis ASAP
Call Poison Control – alkalinization process of urine
       - Prepare bicarb drip – take 1L D5W and remove 150ml and use 3 amps of 50ml bicarb to replace fluid then run at 1.5 times fluid maintenance rate up to a max of 200ml/h.
       - Monitor urine output of 2-3 ml/kg/H – TARGET output
       - Insert a foley – empty urine in the bladder for a baseline for patient's physiology and monitor exact volume and urine testing.
              o Check urine q2h for pH and serum blood gas, potassium, and salicylate levels.

Specific targets are harder to get the more serious the cases (which is why dialysis consideration is so important)

☙ Targets
 Urine pH >7.5
 Serum Potassium < 3.5-5 role is for the urine alkalinization process.
 Serum pH <7.56
 Serum salicylate aims for <2.2 with two continuously declining levels

At the 5–6-hour mark, the repeated serum level was 3.92, and the patient started getting nauseous, diaphoretic, tachypnea, and tinnitus, and resp alkalosis (at worst presentation)
Within 36-48 hours, the patient was treated effectively and resolved all levels. No dialysis was required.


Buffalo Attack

It is a very remote site, a 5-hour drive to tertiary care. Patient is two hours further away from the site.

Buffalo throws the patient to the ground, and the patient lands on his back, the buffalo hits him in the chest with his head, then gores the patient to the left chest (around the 6th rib midclavicular). The patient also gets gored in the back of their legs.
       - Large open chest around 20cm x 10cm following along the rib with lots of red subcutaneous tissue exposed (no sucking chest wound). Concerned for femur fracture in the left leg.

Pt has minimal pain with minimal analgesic (100mcg fentanyl over 2 hours). Spo2 95% HR and BP with in normal limits – no signs of early shock

50yo male with a higher BMI of around 33 and otherwise healthy.
       - ABCs normal. No head or neck pain. Only pain to central chest (not the gaping chest wound) and back pain and pain to the legs

Priorities – transport to greater care.
       - Concern for pneumothorax – ultrasound had no lung slide but doesn’t necessarily mean pneumothorax when you can’t see the two plural lines moving opposite each other.
       - Ultrasound is sensitive to pneumothorax - look for lung point – on ultrasound you can see one side apposition of plura and see it sliding and the other side where you see the absence of sliding. Looking where the visceral pleura is peeling off the parietal pleura. Tracing out the margins of that, you can see how large the air bubble is.
       - He does have a small pneumo – so consider treatment – does patient really need large chest tube? Used small pigtail in this case.

Central chest pain – ultrasound used to look at bony context – found sternal fracture.
Concern for internal bleeding – placed patient in Trendelenburg to see if there was any fluid in the abdomen. It would be caught in the area of the diaphragm to see early detection – nothing major found.
Long bone fracture – linear probe used to follow the cortex of the bone. Not superior to X-rays in long bones. No fracture was noted.
Heart – able to look in subxiphoid and parasternal – no pericardial effusion or mechanical issue. No signs of obstructive or hypovolemic shock.
Within a short period of time, ultrasound was able to rule out very dangerous concerns
CT scan available – verified all found on ultrasound.

Take home points
1. Stay away from wild animals! Fatalities typically come from species that don’t get the attention. It’s typically from the “cute and fuzzy” animals.
2. Consider the amount of force that these animals can cause.
3. ABCs, ATLS and getting pt set up for transport most important.



RxAnestheticTable

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CASE - 28yo female brought in via EMS with GCS 3 who was at a bar with friends and family, she went outside to have a smoke and was found unresponsive (unwitnessed) in the middle of the afternoon. No suspected foul play.

No meds or med hx
Vitals with EMS
P – 88, Spot 98% on RA, T – 36.8, BP – 120/80, R – 16

No known risk factors – no drug use, was out with friends and family had some alcohol.
Well dressed, well groomed, no track marks

Exam: No muscle tone, pupils slightly miotic (but not obvious) but reactive. Full breath sounds, no snoring resp or vomitus. Strong pulses, chest auscultation unremarkable. Abdo is soft, the neck is supple, no obvious trauma, and moist mucous membranes. No spinal concern – no step-off concerns. Good rectal tone. No discernible reflexes 

Appears to be in a deep sleep.

Review ABC’s, IV access, airway stable at present.
BGL – normal, empiric Naloxone – started with .4mg and increased to 1mg up to 2mg no response. 
CT scan – normal - Patient intubated after scan 
Labs – VBG lactate, extended electrolytes – all normal. Tox screen came back after patient intubated with Ethanol  118mmol/L

Consulted with ICU – review of common issues - hypoglycemia, intracranial issues, opioid overdose? None found.

Collateral history - Sister reported to EMS that patient had only been drinking alcohol with no other substances. Reports that patient is a heavy drinker (family unaware)

Sedated with low doses of propofol and fentanyl – patient started waking up quickly and decided to increase sedation while figuring out story. Patient later extubated in ICU once no other concerns cleared and story continued to check out.

Toxic Alcoholism typical concerns:
- Tachypnea – underlying metabolic acidosis – till VBG comes back
- Seizures, especially if serum tox can confirm.
- Serum tox screen ethanol and serum osmolality.
- If no CT - need transport to rule out.


076 - Serotonin Syndrome - Tox 2 miniseries

Case - 32yo male with a history of Major Depressive Disorder(MDD) and taking Sertraline and bupropion.
       - Referred to ED from PCP presenting with loose diarrhea for last 10-12 days – concern for electrolyte abnormalities
       - No complaints of fever, vomiting, abdominal pain, appetite intact, jaundice. No recent travel or sick contacts.
              - Lost a few pounds from having loose stool. 
       - Cognitive fog for 2-3 weeks. Vitals normal with heart rate on the higher end around 94bpm. 

Agitated and slightly tremulous. Dilated pupils and cranial nerves are normal. Skin normal. Has hyperreflexia - No clonus or rigidity

Differentials
Toxidrome, sympathomimetic? Opioid or ETOH withdrawal? Medications? Encephalitis? Hyperthyroidism, any overt electrolyte abnormalities with concern for hypercalcemia *Rhyme Bones, stones, abdominal groans, and psychiatric overtones

Labs – normal, urine drug screen normal. 

Looked like he was hopped up on coffee. Similar presentation to a patient who was on venlafaxine who had a dose change and had serotonin syndrome

This patient's medications were stable with long-term use and no recent changes. 

Categorize serotonin syndrome based on spectrum and adjust treatment accordingly.
       - Mild to moderate presentation – agitated, appears heavily caffeinated, has brisk reflexes, and can have GI involvement.
       - Severe presentation – Hunter Criteria – Hyperthermia, unstable vitals, altered LOC, increased tone in muscles, Clonus. Requires Benzodiazepines

**Antidote – Cyproheptadine 
Have a multidisciplinary approach to treatment - Call poison control, ICU, psychiatry 
 
Recreational drug use – cocaine can be a big precipitation, and opioids (tramadol/fentanyl) can also contribute ** use caution when doing procedural sedation
MDMA or any other serotoninergic agents
Ondansetron, cyclobenzaprine, and dextromethorphan can interact

Patient Management – conservative measures, small dose of benzodiazepines, decreased medications to ½ dosages and ensured good follow-up afterwards. Didn’t want to stop meds completely as they helped with his mental health

Clinical diagnosis – no labs or imaging to confirm.
       - Keep alternative pathology in mind
       - Anticholinergic, EtOH, recreational drugs, hyperthyroidism
       - Hunter Criteria
       - Distinguishing from other etiology’s such as neuroleptic malignant syndrome (NMS) or malignant hyperthermia
NMS – more ridged type presentation vs serotonin syndrome being hopped up on coffee appearance with brisk reflexes and jumpy.
Malignant hyperthermia – typically from recent anesthetic meds in history.

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