Authors: Rory Anderson, Kyle McLachlan, Philippa Evans, Stuart Hamilton, Linzi Clark, Rajesh Chatha / Editors: Rajesh Chatha, Robert Hirst / Codes: SLO10 / Published: 24/12/2021
Merry Christmas from the team in the Southeast Scotland Deanery!
This month’s focus is on the best case reports of the year! Case reporting is a vital way of keeping up to date with the latest practice from across the UK and worldwide in recognising unusual presentations or rare pathologies too small in number to perform large scale trials.
We have waded our way through 1740 case reports from the last twelve months to bring you 11 fascinating ED cases, each with a festive theme. As no Christmas is complete without Christmas Cracker jokes & facts, we’ve added a learning bite to each case report. I’m not going to lie; it’s pretty light on jokes
We hope you enjoy TERN’s Top Papers and have a very happy Christmas and New Year, whether you’re working or have some time to relax.
Ho Ho Ho,
It was around 1pm when a snow ranger noticed a new avalanche had taken place on the hillside. A closer look revealed ski tracks in the snow leading into the crown of the avalanche. He alerted the mountain rescue team just after 2pm, who identified a man buried approximately 70cm below the surface. After great efforts to dig him out from the surrounding snow, this 34-year-old skier was found to have a patent airway with laboured and irregular breathing. He was unable to follow commands and was groaning without audible words (GCS 11). There was no evidence of significant trauma, but it was suspected that he had been submerged in the snow for two hours.
When treating someone with suspected hypothermia, please keep the patient as still as possible
This man stood up against advice and, after standing for up to two minutes, suddenly lost consciousness and had no palpable pulse. The team commenced CPR and continued as they made their way off the mountain. When cardiac monitoring was obtained, he was found to be in ventricular fibrillation. Despite attempts to achieve return of spontaneous circulation with defibrillation, adrenaline and amiodarone, death was confirmed at 4pm.
The key priorities in the management of the conscious hypothermic patient are to avoid further temperature drop and encourage rewarming. In the prehospital setting, simple measures to maintain core temperature include the use of insulating materials and wind barriers and rewarming can be facilitated with heat pads and warm water bottles 2.This case study also outlines the importance of body positioning which, although less intuitive, is equally crucial to prevent further temperature drops and improve survival.
In the hypothermic patient, the extremities have a lower temperature than the heart. Allowing the patient to stand and walk around or even repositioning the patient encourages blood to flow to these cooler peripheral areas which in turn increases the volume of cold blood flowing to the heart 2,3. Further cooling of the myocardium in this way increases the risk of ventricular fibrillation 4, the unfortunate outcome for the man in this case.
A recent guideline produced by the Wilderness Medicine Society 2 puts it well: handle the patient gently, keep them lying flat and avoid moving the extremities.
- Arrest in a Hypothermic Avalanche Victim Completely Buried for 2 Hours. Wilderness & environmental medicine. 2021;32(1):92-97. doi:10.1016/j.wem.2020.10.007
- Dow J, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society Clinical Practice Guidelines for the Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia: 2019 Update. Wilderness & environmental medicine. 2019;30(4):S47-S69. doi:10.1016/j.wem.2019.10.002
- Giesbrecht GG, Bristow GK. A second postcooling afterdrop: more evidence for a convective mechanism. Journal of applied physiology. 1992;73(4):1253-1258. doi:10.1152/jappl.1922.214.171.1243
- Lee CH, Van Gelder C, Burns K, Cone DC. Advanced Cardiac Life Support and Defibrillation in Severe Hypothermic Cardiac Arrest. Prehospital emergency care. 2009;13(1):85-89. doi:10.1080/10903120802471907
From the stars sitting atop Christmas trees to romantic scenes of stargazing on a winter’s night, the star is a familiar symbol of this season. This series of case studies highlights the nephrotoxic effects of the starfruit which, although originating from tropical regions 2, can now be found on the shelves in UK supermarkets. All four patients were male (aged 28, 50, 54 and 55 years old) and had normal baseline renal function. Two of the men had no past medical history, one had a seizure disorder and one had uncomplicated diabetes mellitus. Symptoms started within hours of ingestion and included nausea, vomiting, loin pain radiating to the groin and reduced urine output. All four patients had a severe acute kidney injury (AKI) and two patients required haemodialysis for one week.
Eating as few as 3 starfruits can cause a patient to develop renal failure requiring haemodialysis
Surprisingly, the 50-year-old man with no past medical history required haemodialysis for oliguria and uraemia after consuming only three starfruits. All four patients were discharged from hospital and their renal function returned to baseline within one month.
Why is the starfruit so nephrotoxic? The sour type of this exotic fruit is rich in oxalic acid, which drives interstitial fibrosis and crystallises to cause tubular obstruction 3,4. Movement of these crystals down the ureters is why patients tend to present with renal colic symptoms and, as was the case in these four patients, have evidence of oxalate crystals on urine microscopy 1.
This case series, whilst admittedly only tenuously linked with the Christmas season, highlights the importance of casting the net wide in the patient with an AKI. A number of case reports have identified other important causes of oxalate nephropathy, such as cashew nuts, peanuts, spinach and vitamin C supplements 5-8. A recent article described the case of an 81-year-old man with unexplained renal failure despite extensive investigation. In the end, it came to light that he was incredibly health conscious and had developed oxalate nephropathy after following a high antioxidant diet of “2–3 tablespoons of tomato paste per day, a hand full of Brazil nuts, hazelnuts, walnuts, pistachios, pecans, almonds, several teaspoons of cocoa powder and wheat germ” in addition to a litre of almond milk and high doses of vitamin C 9.
In patients with new AKI consider a diet history as part of your work-up process.
- Herath N, Kodithuwakku G, Dissanayake T, Rathnathunga N, Weerakoon K. Acute Kidney Injury Following Star Fruit Ingestion: A Case Series. Wilderness & environmental medicine. 2021;32(1):98-101. doi:10.1016/j.wem.2020.11.003
- Muthu N, Lee SY, Phua KK, Bhore SJ. Nutritional, Medicinal and Toxicological Attributes of Star-Fruits (Averrhoa carambola L.): A Review. Bioinformation. 2016;12(12):420-424. doi:10.6026/97320630012420
- Fang H-C, Lee P-T, Lu P-J, et al. Mechanisms of star fruit-induced acute renal failure. Food and chemical toxicology. 2008;46(5):1744-1752. doi:10.1016/j.fct.2008.01.016
- Sentís A, Quintana L, Massó E, Peréz N, Botey Puig A, Campistol Plana J. Acute renal failure due to oxalate crystal deposition and enteric hyperoxaluria. Nefrología (English Edition). 2011;31(1):121-123.
- Lamarche J, Nair R, Peguero A, Courville C. Vitamin C-Induced Oxalate Nephropathy. International journal of nephrology. 2011;2011:1-4. doi:10.4061/2011/146927
- Park H, Eom M, Won Yang J, Geun Han B, Ok Choi S, Kim JS. Peanut-induced acute oxalate nephropathy with acute kidney injury. Kidney research and clinical practice. 2014;33(2):109-111. doi:10.1016/j.krcp.2014.03.003
- Bernardino M, Parmar MS. Oxalate nephropathy from cashew nut intake. Canadian Medical Association journal. 2017;189(10):E405-E408. doi:10.1503/cmaj.151327
- Makkapati S, D’Agati VD, Balsam L. “Green Smoothie Cleanse” Causing Acute Oxalate Nephropathy. American journal of kidney diseases. 2018;71(2):281-286. doi:10.1053/j.ajkd.2017.08.002
- Clark B, Baqdunes MW, Kunkel GM. Diet-induced oxalate nephropathy. BMJ case reports. 2019;12(9)doi:10.1136/bcr-2019-231284
After a slightly unhealthy festive period, the gyms are often packed come January. A 54-year-male presented with sudden onset right sided lower abdominal pain associated with a ‘pop’, with urinary urgency, frequency and haematuria but no neurological features. This began whilst he was back squatting 300kg in the gym. He had a past medical history of hypertension, hyperlipidaemia and coronary artery disease. His initial examination findings were bruising to the base of the penis without scrotal swelling, abdominal distension with tenderness and guarding but no signs of peritonitis.
A CT angiogram of his abdomen and pelvis with CT urogram showed a widening of the pubic symphysis to 18mm, small amounts of air in the sacroiliac joints and large intraluminal bladder haematoma. There was contrast extravasation into the bladder and anterior to the prostate into the retropubic space.
Whilst talking to this man, a passing Christmas elf comes along and asks: what is the normal width of the adult pubic symphysis?
You answer “Why, it’s 3-6mm, with minimal movement of up to 2mm shift and 1 degree of rotation allowed.”
Whilst experiencing this festive hallucination, the patient is taken to theatre under urology for cystoscopy and bladder haematoma evacuation. Management of the bleeding was unsuccessful and the patient was transferred to the interventional radiology suite. An arteriogram showed active extravasation of an ‘accessory’ obturator artery, an anatomical variant, arising from the inferior epigastric artery rather than the anterior division of the internal iliac artery. This was coiled with no further extravasation shown.
Unfortunately, the patient continued to experience significant haematuria and was returned to theatre for open exploration leading to repair of a hole in the bladder wall and packing around the prostate. On the patient’s third trip to theatre for removal of packing, the orthopaedic team re-examined the pelvic ring and, finding the pubic symphysis to now be 30mm, the patient underwent plate fixation. The patient was weight bearing as tolerated by 3 months.
How did this happen? Well, whilst attempting to overcome a heavy load on the back (300kg), the patient’s hips underwent forces of excessive external rotation with his legs already hyper-abducted and externally rotated. This created enough tensile stress of the pubic symphysis ligaments to result in complete disruption. The subsequent stress placed upon adhesions between the bladder and nearby small vessel to the pubic symphysis likely led to bladder and arterial injury
The commonest causes of pubic symphysis disruption are:
- Anterior-posterior compression from external blunt force trauma
- Intrapartum or postpartum secondary to spontaneous vaginal delivery and associated with hormonal changes causing lengthening and relaxation of ligament
This case illustrates the importance of pertinent history taking. This patient could have a wide differential for abdominal pain, abdominal distension, and haematuria. However, ensuring that any possible traumatic mechanism, however unusual, is explored when taking the history from the patient aids diagnosis and timely management. Emergency physicians and surgical colleagues should be aware that significant pelvic injuries can occur without significant blunt force trauma.
We should all be aware that we may be somewhat deconditioned on returning to the gym in January and stay on the couch accordingly.
Shieh, Alvin K et al. “Spontaneous pubic symphysis disruption and concomitant bladder rupture during competitive squatting: A case report.” Trauma case reports vol. 27 100299. 18 Apr. 2020, doi:10.1016/j.tcr.2020.100299
An 81-year-old man presents to the emergency department with an acute onset of a painless hoarse voice. He had a past medical history of hypertension and stage IV colorectal adenocarcinoma with pulmonary metastasis. No abnormalities were found on routine cardiovascular or neurological examination. Nasoendoscopy revealed a left vocal cord palsy.
This patient also had a history of aortic arch aneurysm under surveillance. A CXR showed a widened mediastinum and rightward tracheal shift. A CT chest showed a contained aortic aneurysm rupture with an acute hyperdense periaortic haematoma at the aortic arch. This patient was considered a poor surgical candidate in view of his comorbidities and he was managed palliatively.
The differential diagnoses for an acute hoarse voice are:
- Foreign body
- Smoke or toxic gas inhalation
- Ortner’s syndrome
- Acute epiglottitis
- Peritonsillar abscess
Ortner’s syndrome, or cardiovocal syndrome is left recurrent laryngeal nerve palsy secondary to traction or compression of the nerve between the thoracic aorta, primarily the aortic arch, and the pulmonary artery which passes inferiorly.
In an adult patient this is most often caused by thoracic aortic aneurysm, recurrent pulmonary embolism and primary pulmonary hypertension. This is more common in children but should also to be considered in adults with atrial and ventricular septal defects and Eisenmenger syndrome.
Aortic aneurysm rupture can be painless although commonly presents with chest or back pain. It is a fatal diagnosis that often only gets recognised post-mortem or peri-mortem. Because of this, as emergency physicians, our index of suspicion should be high for aortic rupture. Vocal cord disorders can indicate a serious cardiovascular pathology including patent or ruptured aortic aneurysm rather than excessive carol singing.
This case illustrates that left recurrent laryngeal nerve palsy secondary to compression by a thoracic aortic aneurysm may only present upon rupture of the aneurysm. General management would consist of early consideration for surgical intervention and immediate blood pressure control of <120/80 mmHg with a target heart rate of >60 bpm. The first line agents are beta-receptor antagonists: labetalol, esmolol and propranolol. If myocardial ischaemia is present, intravenous glyceryl trinitrate can be added.
This cautionary tale tells us to consider rarer but more serious causes of a hoarse voice.
Lim, Amanda Hui Jun, and Michael Yih Chong Chia. “The Hoarse Voice of an Aortic Aneurysm Rupture: Ortner’s Syndrome.” The Journal of emergency medicine vol. 59,5 (2020): e199-e201. doi:10.1016/j.jemermed.2020.07.014
A 34-year-old man with an unremarkable past medical history is brought to the ED by ambulance with shortness of breath, having been found by family members on the bathroom floor in respiratory distress and with a widespread rash having just gotten out of a hot shower.
On arrival in ED he is maintaining his airway, has reduced breath sounds throughout though without added sounds, is profusely diaphoretic and has diffuse urticaria. He is found to have a blood pressure of 84/60mmHg and a heart rate of 60bpm. Bloods reveal a lactate of 5.3mmol/L, potassium of 2.9mmol/L and a WCC of 12.9cells/mL and are otherwise unremarkable, including a negative troponin. The CXR shows no abnormalities, and the ECG is interpreted as normal sinus rhythm.
Anaphylaxis can be triggered by exposure to the cold
Anaphylaxis, while a life-threatening condition requiring rapid treatment, is one that most EM providers would feel comfortable identifying and managing, though often no trigger is found. Hardy Scots readers considering braving the Loony Dook at South Queensferry this coming 1st January may wish to proceed with caution, as cold temperature can be a rare but clinically significant trigger for anaphylaxis.
As noted in the case report, hypersensitivity to cold temperature has been described in paediatric and dermatology literature but rarely in EM literature. Diagnosis is made typically with provocation tests such as holding an ice cube to the skin for 5 mins and observing for the development of a wheal; and management is largely patient education on cold avoidance and antihistamines (Stepaniuk et al, 2018).
Brevik & Zuckerman (2021) reported this case of a 34-year-old man in Colorado found in anaphylactic shock after stepping out of a hot shower into the cold air of his home. His family reported that he had an “allergy to the cold weather”, having been previously prescribed an adrenaline auto-injector which he had used in response to urticaria triggered by cold weather; though he had not used it on this occasion. Initial pre-hospital management by the paramedics involved administration of O2 and 2 x 0.3mg IM adrenaline and IV diphenhydramine, followed by commencing an adrenaline infusion for refractory shock. In the ED he received IV methylprednisolone, famotidine and normal saline, following which the adrenaline infusion was stopped due to clinical improvement. A positive ice cube test confirmed the diagnosis of cold urticaria, and the patient was prescribed a daily antihistamine along with an adrenaline auto-injector and counselling on the avoidance of cold triggers.
Emergency medicine physicians should be aware that cold temperature could be the cause of otherwise unexplained recurrent urticaria and can be a trigger for anaphylactic shock. Take a thorough history for triggers when taking a history from a patient presenting with anaphylaxis
Brevik, C, and Zuckerman, M “Cold Anaphylaxis: A Case Report.” The Journal of emergency medicine vol. 60,2 (2021): 226-228. doi:10.1016/j.jemermed.2020.09.032
A 50-year-old female self-presents to her local ED on the advice of another health professional. She described symptoms of light-headedness which had been exacerbated by positional changes. The week previously she had symptoms of nausea and diarrhoea. On her arrival to the ED she was asymptomatic.
Past medical history includes previous bacterial myocarditis managed with an LV assist device (LVAD). She regularly takes the medications carveidilol, losartan, and atorvastatin. Her clinical assessment revealed a stable, alert 50-year-old female who was asymptomatic and with moist mucous membranes. Her mean arterial pressure (measured with Doppler) was 50mmHg. Her ECG is as follows:
Patients with an LV assist device have a different cardiovascular physiology
Although this may seem like an unbelievable Christmas miracle, Smith and Moak1 describe a patient with an LVAD presenting to ED relatively asymptomatic who was noted to be in ventricular fibrillation. The patient underwent procedural sedation and defibrillation, successfully cardioverting to sinus rhythm at the second attempt, at 200J. She went on to be commenced on amiodarone and had an implantable cardioverter-defibrillator (ICD) sited.
LVADs are increasingly being used as a bridge-to-transplant therapy for patients with heart failure, or sometimes as a destination therapy. The British Heart Foundation estimates that approximately 100 patients in the UK are currently living with such a device, and around 80 are implanted every year2. LVAD insertion is an open procedure performed in specialist centres; one end of the LVAD pump connects to the left ventricle, and the other end is connected to the aorta. The device is then monitored and controlled externally through a controller. The device is continuous-flow; meaning patients may not have a palpable pulse and may also not have discernible systolic and diastolic pressures. In these patients mean arterial pressure should be measured with a manual cuff and a Doppler device.
As organ perfusion can be adequately maintained by the continuous flow of the device, patients may be able to tolerate ventricular dysrhythmias, as was the case here. Patients with LVADs presenting to the ED should be assessed urgently, and early discussion with an LVAD specialist should be considered. Prompt defibrillation should be considered for LVAD patients presenting with ventricular dysrhythmias. Consideration needs to be given to pad placement, which should be away from the device in the A-P position.
Continuous flow from LVADs can maintain adequate organ perfusion, therefore these patients may tolerate ventricular fibrillation.
- Smith ME, Moak JH. Asymptomatic ventricular fibrillation in continuous flow left ventricular assist device. American Journal of Emergency Medicine 2021; 49: 130-132.
- British Heart Foundation. Focus on: left ventricular assist devices. From: https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/lvads. Obtained on 25/11/2021.
A 54-year-old female presents with chronic abdominal pain and microscopic haematuria. She has had a mild, tolerable but persistent low pelvic pain since the age of 20 and persistent microscopic haematuria. Over the course of her 34-year history of symptoms she has had an extensive battery of investigations without any positive findings, and multiple treatment modalities trialled without any improvement in her symptoms.
During her attendance she is found to have normal observations, normal cardiovascular and respiratory examinations and a normal abdominal examination. She appears systemically well. She has a past medical history of ankylosing spondylitis for which she had been stable on a TNF-α antagonist for the last nine years. Bloods including renal function, ESR, CRP and serum protein electrophoresis were normal.
Her (very astute!) physician arranges for a Doppler ultrasound of the abdomen which demonstrates a marked dilatation of her left renal vein (LRV) with LRV compression in the aortomesenteric space.
The imaging findings are consistent with Nutcracker Syndrome
As well as being a much-loved Christmas classic, The Nutcracker gives its name to an uncommon anatomical variant in which the LRV is compressed as it passes through the junction of the superior mesenteric vein and the aorta. The prevalence is unknown due to the lack of agreed diagnostic criteria and variability of symptoms; however it is an important diagnosis due to the potential for long term LRV hypertension causing chronic kidney impairment and the potential for LRV thromboses.
The symptoms in Nutcracker Syndrome are derived from the outflow obstruction of the LRV, which can give rise to microscopic haematuria, abdominal pain which can be postural and often localised to the left flank or left lower quadrant. As the left gonadal vein drains into the LRV, it can additionally result in testicular pain or varicocele in males, and pelvic congestion syndrome in females (chronic pelvic pain due to ovarian congestion, worsened by posture, intercourse and immediately prior to menstruation).
Diagnosis of the condition is made initially by Doppler ultrasound; CT and MR imaging are often utilised to demonstrate LRV compression, however as non-dynamic modalities these are unable to assess flow through the vein. Management can be conservative, endovascular LRV stenting or surgically with open or laparoscopic LRV transposition or bypass2.
The patient in this case was managed conservatively given the absence of severe pain, renal impairment, macroscopic haematuria or varicocele.
Nutcracker syndrome is an uncommon but important cause of chronic abdominal pain and microscopic haematuria.
- Falsetti L, Martino GP, Mattioli M, Menetti S, Serra C. Chronic abdominal pain and haematuria in internal medicine: do not forget about the Nutcracker syndrome. Internal and Emergency Medicine 2021; 16:443-445.
- Ananthan K, Onida S, Davies AH. Nutcracker syndrome: an update on current diagnostic criteria and management guidelines. European Journal of Vascular & Endovascular Surgery June 2017; 53(6): 886-894.
- By Osmosis – open.osmosis.org (License at end of video), CC BY-SA 4.0
- Getty Images/Corbis Entertainment/Ole Jensen
A 35-year-old male patient presented with a complaint of hiccups that had been going on for fifteen hours. The patient’s hiccups started early in the morning and continued uninterrupted until midnight. He was hiccupping an average of six to eight times a minute. He had drank ice water several times at home, held his breath, swallowed granulated sugar, and bitten lemon, but nevertheless, came to the hospital when these measures proved inadequate. He had a history of twelve hiccup attacks in the last 5 years, which had lasted between twelve and sixty hours. The past attacks had been treated in the hospital with medication. His medical investigation concerning the source of the hiccup attacks revealed no pathology. There was no history of chronic disease or medication use, and he did not use cigarettes and alcohol. His observations were normal. No pathological condition was found in the detailed systemic examination. Routine biochemical tests and complete blood count results were normal too.
There is no clear consensus in the literature on optimal primary medical therapy for persistent hiccups
Chlorpromazine has FDA approval for this use. Metoclopramide is often preferred in the treatment of hiccups. When chlorpromazine and metoclopramide are used together, it usually shows effectiveness within 30 min. However, they can cause different side effects, especially extrapyramidal side effects.
There are many non-pharmacological treatment alternatives for the termination of hiccups. The effectiveness of many physical manoeuvres is based on the hypothesis that stimulation of the pharynx will block the vagal part of the reflex arc, and thus, eliminate hiccups.
Nasopharyngeal stimulation (vinegar, ice application), respiratory maneuvers (Valsalva maneuver, CPAP application), and vagal stimulation (cold application to the face, carotid message) are among the non-pharmacological treatment methods
The patient was treated with esomeprazole, oral sodium alginate. an IV infusion of metoclopramide, and three doses of chlorpromazine hydrochloride infusion. None of which worked so the patient was hospitalized. Since the symptoms did not regress 24 h after the first hiccup attack, it was decided to perform mesotherapy with intradermal injection as an alternative method.
The first intradermal injection was made adjacent to the vagal nerve and the sternocleidomastoid muscle. In this region, the intradermal injection was performed around the sternocleidomastoid muscle according to the course of the vagal nerve. The second injection was directed to the diaphragm, which is the primary muscle responsible for hiccups. Three points were determined in the epigastrium region immediately adjacent to the diaphragm; intradermal injections were applied to these points. The hiccups settled and the patient was discharged without complication.
It is though that this worked through the effect of vagal stimulation on the termination of an acute hiccup.
This paper describes small studies showing the effectiveness of the use of cervical epidural block C3-C5 and phrenic nerve block that did not respond to pharmacological treatment. Intradermal mesotherapy is a more straightforward procedure. Additionally, the risk of developing complications with intradermal injection is lower.
Intradermal injection is potentially a safer alternative to nerve blocks for patients with hiccups resistant to medical treatment.
Kocak, Abdullah Osman et al. “Intradermal injection for hiccup therapy in the Emergency Department.” The American journal of emergency medicine vol. 38,9 (2020): 1935-1937. doi:10.1016/j.ajem.2020.03.044
A 56-year-old man was brought in by EMS after being found unresponsive in a car with a bag of drugs beside him. He was given 0.5 mg naloxone IV by EMS and immediately brought to the hospital. On arrival, the patient was noted to have tight rigidity of his upper extremities, with severe flexion. This presentation was not noted before the delivery of naloxone by EMS.
Be cautious when using synthetic opioids of wooden chest syndrome
This paper describes case reports have highlighted the rare side effects of chest wall rigidity or “wooden chest syndrome” with fentanyl and other opioid agonists. It is commoner with synthetic agonists. The effect on the chest is that it decreases compliance and functional residual capacity, thus worsening the ability for a patient to effectively ventilate. This was the first case report describing the syndrome with naloxone.
Wooden chest syndrome is rare side effect of synthetic opioid agonists. This is the first case report to describe it with Naloxone.
Levine, Rykiel et al. “Wooden chest syndrome: Beware of opioid antagonists, not just agonists.” The American journal of emergency medicine vol. 38,2 (2020): 411.e5-411.e6. doi:10.1016/j.ajem.2019.09.009
A 10-year-old female patient presented to the Emergency Department for evaluation of burn to palm and fingers of her left hand. Patient reported she began playing with homemade “slime” five days prior and had been progressively developing blisters in the palmar aspect of her hand.
On examination of the patient’s skin, the patient had a non-circumferential burn to the palmar aspect of her left hand overlying her palm as well as digits one through four. Overall, the patient had less than 1% total body surface area burns. The patient had limited flexion of fingers due to large tense bullae, but otherwise normal neurovascular exam. The patient’s hand was copiously irrigated, and wound care was performed in ED. Patient’s vaccines were up-to-date and there was no need for tetanus prophylaxis. Burn surgeons were consulted and arranged for the patient to be brought to the operation room the following morning.
Borax or boric acid is the active ingredient in slime products making the substance pliable and is commonly noted as the culprit in slime toxicity.
Slime is back in fashion as a toy. It is a type of modelling dough with various types of appearances and textures. It is both commercially available and can also be manufactured at home. Slime is made from a combination of household items including white school glue (polyvinyl acetate glue), water and boric acid
Borax has a pH of 9.0 which can cause liquefactive necrosis which is typical of alkali burns. Most reported adverse event of slime exposure is an irritant contact dermatitis, where patients are instructed to stop handling product and discharged home with topical corticosteroids In this particular case, the adverse event associated to the exposure was much more severe.
Homemade slime contains Borax which is an alkaline substance capable of causing chemical burns
Guzman, Karla, and Isabel Brea. “Do-it-yourself slime: A novel cause of pediatric burns.” The American journal of emergency medicine vol. 38,10 (2020): 2247.e3. doi:10.1016/j.ajem.2020.05.067
A 65-year-old man who had previously undergone total arthroplasty of both hips was admitted to the hospital after a fall resulted in the dislocation of his right hip. He had no other injuries from the fall. A handheld Doppler device was used to assess the pulses in his feet. When the probe was placed on the dorsalis pedis of either foot, music could be heard from the device speaker in addition to the pulse. This outcome occurred each time that the dorsalis pedis pulse was assessed in either foot and persisted when other handheld Doppler devices were used. The same Doppler devices did not receive music when used on hospital staff members.
Dopplers may experience interference from radiofrequencies.
It was thought that the Doppler may have picked up a radio signal being received by one or both of the patient’s prosthetic hips, although other equipment in the room (such as the hospital bed) could have received the signal.
Findings such as these should be reported to the facility’s engineering department for further investigation. In this case, no faulty equipment was identified. Eight months after this event, the patient was doing well and had had no further falls.
There really isn’t one we just thought it was fun! Merry Christmas everyone and thanks for reading!
Wise L. “Hearing Music while Checking a Pulse.” New England Journal of Medicine 383.26 (2020): e139. Ovid MEDLINE(R). Web. 14 December. 2021