Mechanical Ventilation in Shock

• Emergency physicians and intensivists routinely resuscitate patients in shock.
• For patients who manifest signs of persistent shock (i.e., rising lactate), consider intubation and mechanical ventilation, even in the absence of acute respiratory failure.
• The respiratory muscles are avid consumers of oxygen.  In fact, up to 50% of available O2 can be used by the respiratory muscles to perform the work of breathing.
• Initiation of mechanical ventilation can reduce oxygen consumption and allow oxygen to be shunted to other vital organs.

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Parsonage Turner syndrome aka Neuralgic amyotrophy

 

30 cases per 100,000

Under recognized and often missed

Unknown cause, perhaps post viral. Also reported post stress (surgery, pregnancy)

Can be B/L in 10 to 30%

CC: sudden onset of severe pain in the shoulder.

Can last for hours to weeks.

Radiates to upper arm.

As pain begins to subside, muscle weakness and sensory loss follows.

Can preferentially involve the suprascapular and axillary nerve.

Outpatient workup may include MRI and EMG

Treatment: Supportive. Consider a trial of oral steroids. Provide good pain control.

Majority of patients improve within 3 months. Though up to a third have persistent pain/functional deficit.

Many medications are discovered from plants (quinine – cinchona trees) or organisms (penicillin – mold [penicillicum]).

Digoxin was isolated from foxglove (Digitalis lanata), a colorful floral plant often found in many gardens.  There are other sources of cardioactive steroids (aka cardiac glycosides) that have similar effect as digoxin.

• Oleander (Nerium oleander)
• Yellow orleaner (Thevetia peruviana) – frequently used for suicide in Southeast Asia
• Lily of the valley (Convallari majalis) – use in wedding bouquet
• Dogbane (Apocynum cannabinum)
• Red squill (Urginea maritima)
• Bufo toad (Bufo species)  

 

Non-digoxin cardioactive steroid exposure can result in a positive digoxin level due to cross reactivity. This confirms exposure; however, the “digoxin level” does not represent the true extent of the ingested dose or toxicity. 

Non-digoxin cardioactive steroid toxicity

• Digibind also binds to non-digoxin cardioactive steroids.
• However, larger doses are often required (initial dose: 10 to 20 vials) than doses required for digoxin toxicity.   

• A retrospective single center study reviewed 788 patients who presented to the ED with concern of stroke and found 21 (3%) patients had only aphasia symptoms by the NIHSS.
• None of these patients had evidence of infarct on neuroimaging.
• 3 of these patients were diagnosed with possible transient ischemic attack (TIA) though also had other possible diagnoses.
• Toxic/metabolic disturbances (39%), followed by seizure (11%), syncope (11%), and chronic medical problems (11%) were the most commonly diagnosed stroke mimics.

Take Home Point: This small but interesting study looked at the incidence of isolated aphasia presenting for concern of stroke. They found that none of their patients had evidence of an infarct, suggesting that strokes affecting language without motor or sensory deficits are uncommon.

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Should that patient be admitted to the floor? 

Several studies have evaluated factors associated with upgrade in admitted patients from the floor to an ICU within 24 or 48 hours. Elevated lactate, tachypnea, and "after-hours" admissions have been repeatedly identified as some of the risk factors for decompensation. 

Two recent studies tried again to identify predictors of eventual ICU requirement...

Best predictors of subsequent upgrade:

• Hypercapnia*
• Tachypnea (in sepsis patients)*
• Hypoxemia (in pneumonia patients)
• Nighttime admission
• Initial lactate ≥ 4

The most common reasons for upgrade:

1. Respiratory failure
2. Hemodynamic instability

Effect on mortality? 

Despite a more stable initial presentation, mortality of patients who decompensated on the floor (25%) matched that of patients initially admitted to the ICU.

*One of the studies noted that although respiratory rate was demonstrated to be the most important vital sign, it was missing in 42% of the study population, while PCO2 was only obtained in 39% of patients.

Bottom Line: 

• Make sure to physically reassess patients you've stabilized/improved in the ED with current vital signs (including an accurate respiratory rate!) before okaying their admission/transfer to the floor. 
• If you get a blood gas, make sure to pay attention to the PCO2 and address any abnormalities appropriately.

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Strategies for Hyperkalemia Management
Stabilize cardiac membrane	Calcium gluconate
Intracellular movement in skeletal muscles	Albuterol Sodium Bicarbonate Insulin
Potassium excretion	Loop Diuretics Kayexalate Patiromer (chronic use only)
Potassium removal	Dialysis

 

Insulin mechanism of action for hyperkalemia:

· Binds to skeletal muscle receptors

· Increased activity of the sodium-potassium adenosine triphosphatase and glucose transporter GLUT4

· Glycemic response occurs at lower levels of insulin

· Potassium transport activity increases as insulin levels increase

Patients with insulin resistance due to type-2 diabetes do not become resistant to the kalemic effects of insulin.

 

Hypoglycemia following insulin administration for hyperkalemia:

· Occurs 1-3 hours post dose, even with initial bolus of dextrose

· The amount of glucose is insufficient to replace the glucose utilized in response to the administered dose of insulin

· Insulin’s half-life is increased in ESRD leading to longer duration of action

 

A systematic review of 11 studies regarding insulin dosing for hyperkalemia:

· 22 patients (18%) experienced hypoglycemia

· Studies that only gave 25 grams (1 amp) of dextrose had the highest incidence of hypoglycemia (30%)

 

Tips:

· Consider insulin dose reduction in patients with renal failure

· Use an order set to ensure patients receive appropriate POC glucose monitoring to detect delayed onset of hypoglycemia

· Dextrose 50% (25 grams) should be given to all patients with pre-insulin BG <350 mg/dL

Subsequent PRN dextrose 50% (25 grams) should be used to maintain BG >100 mg/dL after insulin administration

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Core Temp <32 degrees leads to impaired shivering and confers increased risk for malignant ventricular dysrhythmias. Core Temp <28 degrees substantially increases risk of cardiac arrest. 

 

If in cardiac arrest:

• VA ECMO. Rewarming rate ~6 degrees per hour.
• Cardio Pulmonary Bypass. Rewarming Rate ~9 degrees per hour.
• Consider transfer to center with ECMO or CPB capabilities
• Consider up to 3 defibrillation attempts for shockable rhythm
• Consider with holding epi until core temp >30 degrees and doubling interval between doses (q6-10 minutes) until core temp >35 (European Resuscitation Council recs – note this differs from AHA guidelines/recommendations)

 

If perfusing rhythm:

• Institute active external rewarming (warm environment, forced-air heating blankets, arctic sun, warm parenteral fluids). Rewarming Rate ~ 0.1-3.4 degrees per hour.
• Consider minimally invasive rewarming with TTM cooling/rewarming catheter (Alsius/Zoll) via femoral vessel. Rewarming Rate ~3.5 degrees per hour.
• Hemodialysis or CRRT can be considered if intravascular rewarming device unavailable. Rewarming rate 2-4 degrees per hour.
• Avoid IJ or SC central lines, rewarming catheters, and HD catheters -- myocardial irritation with wire/catheter may precipitate ventricular dysrhythmia.

 

Consider addition of more invasive rewarming techniques in those with hemodynamic/cadiac instability or without access to VA ECMO/CPB:

• Thoracic lavage. Rewarming rate ~ 3 degrees per hour
• Peritoneal lavage. Rewarming rate ~ 1-3 degrees per hour  
•  

Consider stopping resuscitation efforts if/when:

• K >12- suggests hypoxia before cooling, no reported survivors. Some recommend K of 10 as cutoff in adults.
• Rewarmed to 32 degrees and no signs of life.

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The cornerstone treatment of poisoning is removal of the toxin from the patient. This can be accomplished before absorption into the body by decontamination methods (dermal or gastrointestinal) or after absorption by blocking metabolism of parent compound, displacing drugs from receptors, binding toxins with neutralizing agents (chelators, Fab fragments), or enhancing elimination by dialysis. Toxins that are ideal candidates for dialysis include substances that are low molecular weight, have low volume of distribution (stay in the blood stream), or low protein binding. Toxins most commonly treated with dialysis are:

• Lithium
• Salicyclates
• Ethylene glycol
• Methanol
• Acetaminophen

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Question

Quadriceps Contusion

Mechanism: Blunt trauma to the anterior thigh (frequently football helmet or opponents knee)

Usually involves the anterior quadriceps (rectus femoris and vastus intermedius)

Pain on passive stretch and active contraction

Can develop large hematomas

Loss of knee flexion is a poor prognosticator

Complication: Myositis Ossificans (MO) (5-17%)

               Increased risk with delay in treatment > 3 days

               Radiographs can lag. Ultrasound in more sensitive

               Painful firm area in region of contusion occurring 2 to 3 weeks post injury

http://fifamedicinediploma.com/wp-content/uploads/2015/12/myositis_ossificans_lateral-1.jpg

Prompt treatment….key to good outcome and earlier return to sports

Large hematoma can be aspirated. NSAIDs may reduce edema and risk of MO. Splinting

Place quadriceps in 120 degrees of flexion for 24 hours following injury (keep muscle lengthened)

https://upload.orthobullets.com/topic/3103/images/quad%20contusion_moved.jpg

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Some pediatric practitioners have adopted the oxygenation index (OI) ([FiO2 × mean airway pressure (Paw) × 100]/ PaO2) or oxygen saturation index (OSI) ([FiO2 × Paw × 100]/ SpO2) to assess hypoxemia in children instead of P/F ratios because of the less standardized approach to positive pressure ventilation in children relative to adults. 

OI can be used in pediatric patients to define severity of Acute Respiratory Distress Syndrome (ARDS) in patients receiving invasive mechanical ventilation and assess for potential ECMO treatment. 

In contrast, the P/F ratio should be used to diagnose Pediatric ARDS for patients receiving noninvasive continuous positive airway pressure [CPAP] or bilevel positive airway pressure [BiPAP]) with a minimum CPAP of 5 cm H2O.

Oxygen Index (OI) = FiO₂ x MAP x 100
                                 ---------------------
                                         PaO₂

• Mild ARDS: 4 ≤ OI ≤ 8
• Moderate ARDS: 8 ≤ OI < 16
• Severe ARDS: OI ≥ 16

• OI < 25: good outcome
• OI 25-40: >40% mortality
• OI > 40: Consider ECMO

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Her first book “The mysterious affair at Styles,” Agatha Christie introduced her lead detective in her novels, Hercule Poirot - the Belgian detective.  She also described the death of Mrs. Emily Inglethorp by strychnine.

Strychnine is found in a disc-like seed of strychnos nux-vomica, a tree native to tropical Asia and North Australia.

It is currently used as rodenticide (moles and gophers), in Chinese herbal medicine and a traditional remedy in Cambodia.

Strychnine inhibits binding of glycine (a major inhibitory neurotransmitter in spinal cord) to Cl-channel resulting in identical clinical syndrome – seizure-like generalized muscle contraction with normal mental status – as tetanus toxin. Tetanus toxin inhibits the release of presynaptic glycine in the spinal cord. 

 

Management

Goal: decrease muscle hyperactivity

• 1^st line: benzodiazepine
• 2^nd line: barbiturates or propofol
• 3^rd line: paralysis by non-depolarizing agents

It's respiratory infection and flu vaccine season! Time to brush up on Guillain-Barré Syndrome..

- It is the most common cause of acute or subacute flaccid weakness worldwide

- 70% of cases are preceded by an infection in the past 10-14 days, but most are minimized or forgotten by the patient. 40% of these infections are by Campylobacter jejuni.

- 30% develop respiratory failure requiring intubation and ventilation

- Half of the patients will develop their maximum weakness by 2 weeks, most will develop it by 4 weeks.

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Infectious Diarrhea:

Have your wondered what you should do with patients that you suspect have infectious diarrhea. Well the IDSA has updated their 2001 guidelines for the management of infectious diarrhea. The TAKE HOME Points are:

• Most patients with diarrhea do not need to be tested for an infectious cause. Stop ordering those cultures.
• Testing IS recommended in the folllowing populations:
  • Patients younger than 5 years
  • Elderly
  • Patients that are immunocompromised
  • Patients with bloody diarrhea
  • Patients with severe abdominal pain or tenderness, or have signs of sepsis.
  • Testing may be considered for C. difficile in people >2 years of age who have a history of diarrhea following antimicrobial use and in people with healthcare-associated diarrhea
• Some additional recommendations that are noteworthy:
  • Fecal leukocyte examination and stool lactoferrin detection should NOT be used to establish the cause of acute infectious diarrhea
  • A peripheral white blood cell count and differential and serologic assays should NOT be performed to establish an etiology of diarrhea
  • Reduced osmolarity oral rehydration solution (ORS) is recommended as the first-line therapy of mild to moderate dehydration in infants, children, and adults with acute diarrhea from any cause

 

You can find all the recommendations at https://academic.oup.com/cid/article/doi/10.1093/cid/cix669/4557073/2017-Infectious-Diseases-Society-of-America

 

 

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Within the first hour after administration, ondosterone, metoclopramide and bromopride were equally efficacious.  At the 6 hour and 24 hour period after receiving the initial dose of medication, ondansetron was statistically superior to bromopride (not available in the US) and metoclopramide.  There were no reported side effects in the ondansetron group (including diarrhea or sedation).

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Agatha Christie is an English crime novelist who frequently used poisons in her books to murder the victims. In her book, Murder is Easy, Ms. Christie uses arsenic/arsenic trioxide to kill several characters.

 

Primary source of arsenic in general population is contaminated food, water and soil. Arsenic exists in several forms: elemental, gaseous (arsine), organic and inorganic (trivalent or pentavalent).

 

Arsenic trioxide has also been used to treat acute promyelocytic leukemia in China; it’s use in other leukemia, lymphoma, and other solid tumors are currently being investigated.

 

Arsenic primarily inhibits the pyruvate dehydrogenase complex and multiple other enzymes involved in the citric cycle/oxidative phosphorylation, resulting in mitochondrial dysfunction.

 

Acute toxicity of arsenic after ingestion

1. GI symptoms (minutes to several hours) – nausea, vomiting, abdominal pain and cholera like diarrhea.
2. Cardiovascular: QT prolongation/torsade de pointes, orthostatic hypotension, ventricular dysrhythmias, myocardial dysfunction and shock.
3. CNS (days): encephalopathy, delirium, coma, and seizure due to cerebral edema and microhemorrhages.
4. Respiratory: ARDS, respiratory failure,
5. Others: AKI, leukemoid reaction, hemolytic anemia, and hepatitis.

 

 Management

1. Chelation: dimercaptrol (BAL) or succimer
2. Whole bowel irrigation if radiopaque material is present (abdominal XR)
3. Electrolyte and fluid management
4. Cardiac monitoring and pressor support in hypotension

Improving CPR Performance

• High-quality CPR is the cornerstone of successfull resuscitation from cardiac arrest.
• In fact, high-quality CPR is considered the most important intervention for achieving ROSC and good neurologic recovery.
• Pearls for optimizing CPR performance include:
  • Use a team-focused approach
  • Avoid leaning and ensure complete recoil of the chest
  • Target a chest compression fraction of at least 60%
  • Use POCUS, but pay attention to the duration of hands-off time
  • Target ETCO2 of > 20 mm Hg

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Complete or incomplete separation of the articular cartilage and subchondral bone

               -70% occur at the lateral aspect of the medial femoral condyle

               -Also seen in the talar dome and capitellum

Repetitive overloading leads to fragmentation and separation from surrounding bone

Prognosis better in kids than in adults

http://www.eorif.com/KneeLeg/Images/OCD4w.jpg

CC: Vague difficult to localize activity related pain and swelling. Mechanical symptoms only if loose body is present

PE: Wilson’s test

Internal tibial rotation and knee extension impinges the tibia on the OCD lesion causing pain. Pain abates with external rotation and flexion.

https://www.youtube.com/watch?v=e7zrKo41Pos

Plan of care: Limit activity and trial period of non-weight bearing for 6 weeks.

50% resolve in 10 to 18 months with conservative care.

Detached, loose or unstable fragments or failure of non-operative care will need surgery

Pediatric patients are at a higher risk of blunt renal injury due to multiple anatomic features, include relatively less protective perinephric fat and surrounding musculature, and larger size of the kidneys in relation to the abdomen compared to their adult counterparts (1). For this reason, it is important to keep a high clinical suspicion for renal injury in the pediatric patient with blunt abdominal trauma, particularly in those with lower rib fractures, direct injury, flank ecchymosis and/or tenderness, rapid deceleration injury, or other significant traumatic mechanism (2). Despite the risk of radiation exposure, the preferred imaging modality for the diagnosis of renal injury in pediatric patients is computed tomography (similar to adults). Studies evaluating the utility of renal ultrasound have demonstrated poor sensitivity with a decreased likelihood of diagnosing low-grade injuries. While ultrasound may be a useful screening tool to evaluate for severe injury, it should not be used to rule out traumatic injury (1). Take home point: Keep a high suspicion for renal injury in pediatric patients with blunt abdominal trauma and confirm the diagnosis with computed tomography of the abdomen and pelvis with contrast.

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Cannabinoid hyperemesis is a syndrome (CHS) characterized by severe intractable nausea, cyclical vomiting, and abdominal pain associated with chronic marijuana abuse. It is often a underrecognized cause of cyclic vomiting syndrome. Despite well established anti-emetic properties of marijuana, paradoxical effects on the GI tract exist through cannabinoid receptors which exert their neuromodulatory properties in the central nervous system and the enteric plexus. Multiple theories of mechanism of CHS are in the literature. Diagnosis is based on the following clinical criteria:

• History of regular cannabis for any duration of time
• Refractory nausea and vomiting
• Gastrointestinal evaluations fail to identify other clear causes
• Compulsive bathing in hot water temporarily alleviates symptoms often done several times a day. A red flag symptom.
• Resolution of symptoms after cannabis is discontinued

Acute care goals are to treat dehydration and terminate nausea and vomiting. Administration of intravenous fluids, dopamine antagonists, topical capsaicin cream, and avoidance of narcotic medications are recommened treatment measures. Benzodiazepines followed by haloperidol and topical capsaicin are reported to be most effective. Capsaicin  activates the transient receptor potential vanilloid 1 receptors (TRPV1) which impairs substance P signalling in the area postrema and nucleus tract solitarius similar to noxious stimuli, such as heat. 

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