Author Archives: daniel frick

Don’t Inhale

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Had an interesting case recently while I was working at Jewish Downtown. Approximately 50s male presents in acute respiratory distress. Apparently he rented out some apartments and one of the tenants clogged one of the toilets, I didn’t have a chance to ask how.

Anyway, in an attempt to fix the problem he mixed two plumbing agents: Liquid Fire Drain Opener & some other generic drain-o liquid that he planned to use to clear the pipes. This ended up being a bad idea and a chemical reaction occurred releasing a cloud of chlorine gas. The patient inhaled this and began becoming progressively more short of breath.

While en route, EMS initially had him on a nasal cannula but transitioned him to a non-rebreather as well as a Duo-neb. At the time of his arrival to room 1 the patient was in obvious respiratory distress, diaphoretic, and anxious pulling at the non-rebreather and leads. His O2 sat was from 86%-88% on the non-rebreather with decreased breath sounds diffusely. We elected to intubate the patient with etomidate as our induction agent and rocuronium as our paralytic. After the patient was placed on the ventilator we started the patient on nebulized sodium bicarbonate.

This was something I had never done before – so I wanted to discuss chlorine gas inhalational injuries and the role of nebulized bicarb.

Chlorine gas inhalations typically occur in the setting of chemicals for cleaning an indoor pool. Chlorine gas inhalation rarely progresses to respiratory distress requiring intubation.

In 1994 the Journal of Clinical Toxicology did a two year retrospective review of 86 cases of chlorine gas inhalation and none of the patients progressed to respiratory insufficiency requiring ventilator support.  The most common symptoms are cough, chest pain, and shortness of breath and the chest xray is often unrevealing. In the study all 86 cases received nebulized sodium bicarbonate and none of the patients clinically deteriorated or acutely worsened as a result of the treatment.

While the nebulized bicarb does not reverse or work to eliminate the inhaled chlorine, it helps symptomatically with the cough and SOA. I could not find much information on the MOA or science behind the use of nebulized sodium bicarbonate but it appears to be pretty safe.

The dosing that I found is 4mL of 4% nebulized NaHCO3, and be prepared to explain this to the respiratory therapist because this is not something that they do often. Also this has to come up from pharmacy as code cart sodium bicarb is typically 7.5% so the concentrations are different.

So our patient received his nebulized bicarb once it came up from pharmacy. He was admitted to the ICU and I have not had a chance to follow up on his outcome yet. I just thought this was an interesting case and something that I had not yet encountered and figured I would share for your reading pleasures.

Approach to the Fussy Infant

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There are many different types of challenging patients that we all dread seeing when they pop up on the board. Whether the patient’s chief complaint is headache, back pain, or pregnant female with abdominal pain. Another very challenging patient presentation is the crying infant. The differential when evaluating a crying infant is broad. In this post I will include a list of differential diagnosis to consider based on organ system and then a patient I had that presented in this way.

CNS- Meningitis, epidural hematoma, subdural hematoma, hydrocephalus

HEENT- Skull fracture (accidental or non- accidental trauma), ocular foreign body, corneal abrasion, otitis media, nasal foreign body.

Cardiovascular- SVT, myocarditis, congestive heart failure

Pulmonary- foreign body in airway, bronchiolitis, pneumonia

GI- Malrotation/volvulus, pyloric stenosis, appendicitis, gastro-esophageal reflux, intussusceptions, anal fissure

GU- Testicular torsion, UTI, incarcerated inguinal hernia, soap vaginitis, phimosis, paraphimosis

Musculoskeletal- Fracture, septic arthritis, dislocation, hair tourniquet

My patient presented as a 1 month old male with his Spanish speaking Hispanic parents. Mom stated that he has been crying consistently for the past 4 days. She does not remember a specific time when the crying started but she states it has not improved.

Mom is breastfeeding the baby and denies any dietary changes. The baby was full term and mom had no complications with the pregnancy. Patient up to date on all vaccinations. Baby has been afebrile and per mom has not been lethargic. Baby is still feeding well and gaining weight appropriately and mom denies any projectile vomiting after feeds, denies any change in stooling, and notes good urine output. Baby lives at home with mom and dad and I have no red flags to suspect non-accidental trauma.

On exam he is overall well-appearing and does not appear to be in any type of distress: crying but consolable. He appeared to be healthy. He was interactive, tracking me with his eye movements, and did not appear to be meningitic or lethargic. Heart and lungs were unremarkable and abdomen was soft, nontender and non distended. GU exam (make sure you do this) was unremarkable. Baby was moving all extremities while lying on the oversized adult bed in the middle of the hallway and on inital exam did not appear to have any outward bruising or signs of trauma.

Upon removing the patient’s socks I noticed something odd on his second toe of his right foot. Just distal to his PIP joint he had a circumferential red line. As soon as I started to examine that toe his crying increased substantially. On further examination he had a hair tourniquet that had eroded its way all the way down to the bone of the middle phalanx of the second toe.

At this point the baby was still in the hallway and we took him to Room 9 to attempt to try any remove it. I am sure you can imagine how awesome this was on a crying kicking 1 month old. We attempted to unwind the hair but ultimately were unable to do so as it was just to deep into the tissue. I called Kosair and the patient was transferred and I do not yet follow up on the final outcome.

This just re-enforces the importance of a good head to ahem, toe physical exam on patient’s that are not straight forward. Mom had been with the infant 24/7 for the past 4 days and had not noticed this; not to mention who knows when the hair tourniquet actually started. Just something to keep in mind and hopefully this helps next time you all have to examine a crying baby.

 

Hypotension

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Late 70s year old female with chief complaint of dizziness and fatigue. Patient has a medical history of HTN and recent cataract surgery.  In triage patient was hypotensive with BP of 70\35 and Bradycardic with a heart rate ranging from 55-60, O2 sats 100% on room air and afebrile.

I found the patient to be lethargic. Otherwise her exam was unremarkable with no focal neurologic deficits, cardiac and pulmonary exam unremarkable, and no abdominal pain. Her husband was in the room and states that they were on their way to their grandson’s high school graduation and she began complaining of feeling dizzy and she started to become lethargic. She had not been sick recently and before this morning she was completely at her baseline. To note yesterday her blood pressure was 180/95 when she checked at home so she typically runs high. No new changes to her medications which consisted of metoprolol Succinate 100mg QD and a Baby Aspirin.

As I talked to the husband he went on to explain that she had recently had cataract surgery on her left eye and that this morning she had a follow up appointment with her ophthalmologist. While at the ophthalmologist appointment the doctor said that the pressure in her eye was high and she received some drops in her eye to bring the pressure down but the husband could not remember the name of the drops.

So I started by getting CBC, CMP, TSH, Urine, Chest xray, EKG, Troponin and a head CT to complete my little old lady AMS workup. Obviously the differential diagnosis for AMS in the elderly is vast so I was considering a lot of different possibilities.  While I waited for her results to come back I called her Ophthalmologist that she had seen that morning to see what drops she had received. Ends up she got Alphagan which is an alpha agonist, Trusopt which is a carbonic anhydrase inhibitor, and 3 drops of Timolol. I discussed with him the possibility of the Timolol on top of her morning metoprolol 100mg as potentially causing her hypotension and bradycardia. He stated he had never seen that happen in his 16 yrs of practice but it is theoretically possible. A quick Uptodate search confirmed that hypotension can occur in as many as 10% of patients using Timolol eye drops which to me was a surprisingly high number.

So I’ll go ahead and cut to the good stuff. All of her labs and imaging returned unremarkable and her EKG just showed sinus bradycardia with a rate of 57.  Ultimately she got 2L of Normal Saline and we watched her for about 5 hrs. Throughout her stay her blood pressure steadily increased and at the time of her discharge she was 135/86 with a heart rate of 74 and she was back to her baseline and much more awake.

I thought this was an interesting case as it seems relatively rare for topical eye drops to result in systemic side effects however in the right patient population it can result in severe side effects. A quick literature search brought up multiple case reports of patient’s having symptomatic bradycardia and even syncope resulting from Timolol use.

So definitely something to keep in mind if you have a elderly or frail patient with acute angle glaucoma who is already on beta blocker therapy. Maybe trying other drops first instead of Timolol or at least be sure to make the patient aware of the possibility of side effects including hypotension, bradycardia, fatigue, and even syncope so they know what to watch out for.

The elusive S1Q3T3

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So this is a case I thought was interesting that I had in the department back in May. We all know that the most common EKG finding in the setting of PE is sinus tach, however the pimp question that is also asked is the finding of S1Q3T3. While I can easily recite the alphabetic-numeric code S1Q3T3 by heart at the drop of a hat, I had never seen one and honestly thought I never would. I thought finding S1Q3T3 was likely as rare as surviving a ED thoracotomy (OK maybe not that rare).  So on to the case.

39 year old female presents to the ED complaining of SOA and cough for the past two weeks. Cough was productive of green sputum, no fevers, and she does complain of some chest pain which sounds pleuritic in nature. Initial vitals HR 118 BP 111/73 RR 16 O2 97% room air. As I get into her PMH she says she has a history of multiple PEs with an IVC filter placed 1 yr ago because apparently she wasn’t very good at remembering to take her coumadin. She has had a hypercoagulability workup which was negative, no recent travel, no estrogen use.

So at this point with a history of multiple PEs, tachycardia, SOA, and pleuritic chest pain I am thinking I am going to scan this lady. Even though she had a IVC placed a year ago, she is still saying all the right things for PE. So while the CTPE protocol was cooking I got an EKG and there it was, S1Q3T3!

S1Q3T3

Needless to say I was pretty excited and immediately showed the rotating intern next to me who clearly didn’t share my enthusiasm. When I compared this new EKG to a past EKG a month ago she did not have the S1Q3T3.During her admission a month ago, when she had a normal EKG, she had a CTPE showing a chronic PE. This time when her CTPE came back the read was Acute on Chronic Pulmonary Embolism. So a month ago she had a chronic PE with a normal EKG and at this visit she had an EKG with S1Q3T3 and a acute on chronic PE. Out of curiosity I dug through her medical history a little bit more and found that this patient had multiple prior admissions for PE with multiple CTPE protocols and EKGs. What I found was that whenever this patient had a CT read of Chronic PE she had a normal sinus rhythm EKG. However, whenever she had a read of Acute on Chronic PE (which was 4 times!) she had a EKG showing S1Q3T3, dating all the way back to 2012. Yea, apparently this lady has been hanging out with a chronic PE in her distal right main pulmonary artery since 2012 and every once in a while she will throw a new small PE, even with an IVC filter.

So after doing a little bit of thinking and a little bit of reading it made sense. The EKG finding of S1Q3T3 is indicative of right heart strain, in this case resulting from an acute PE. So this patient’s heart has adapted to her chronic PE, however every time she throws a new PE she has an element of right heart strain which can be seen on her EKG as S1Q3T3.

I just thought this was pretty interesting to actually see the physiologic and mechanical adaption and strain this patient’s heart was undergoing being clearly demonstrated on her EKG. Also I learned that S1Q3T3 is not like a q wave after an MI in that it stays on the patient’s EKG, it is a finding that comes and goes depending on the patient’s presentation.

Anyways I thought this was a pretty cool little case and figured I would share. Hope you all enjoyed.