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Medscape
15-07-2025
- Health
- Medscape
A Comatose Patient's Urgent Return to the ED
Editor's Note: The Case Challenge series includes difficult-to-diagnose conditions, some of which are not frequently encountered by most clinicians, but are nonetheless important to accurately recognize. Test your diagnostic and treatment skills using the following patient scenario and corresponding questions. If you have a case that you would like to suggest for a future Case Challenge, please email us at ccsuggestions@ with the subject line "Case Challenge Suggestion." We look forward to hearing from you. Background A 42-year-old comatose man is brought to the emergency department (ED) by ambulance. He had recently been hospitalized for decompensated hepatitis C virus liver cirrhosis at another hospital, from which he left against medical advice. In the hours before admission to the ED, the patient experienced two witnessed episodes of loss of consciousness associated with urinary incontinence and myoclonic jerks. The patient's prescribed medications include abacavir, lamivudine, and zidovudine daily for HIV infection. He also takes furosemide (50 mg), potassium canrenoate (an aldosterone antagonist), lorazepam, and methadone (90 mg); the latter is for the management of heroin addiction. Physical Examination and Workup Upon physical examination, the patient is lethargic, and his Glasgow Coma Scale score is 6 (eye opening response, 1; verbal response, 1; motor response, 4). His pupils are normal in size and bilaterally reactive to light. He has a temperature of 96.8°F (36.5°C), a blood pressure of 90/54 mm Hg, and a pulse rate of 86 beats/min. His respiratory rate is 18 breaths/min, and he has an oxygen saturation of 98% while breathing room air. Upon auscultation, the lung fields are clear bilaterally, and normal heart sounds are heard. His peripheral pulses are palpable; however, bilateral lower extremity pitting edema is present. The abdomen is distended, tense, and with ascites. His sclerae are noted to be icteric. Laboratory tests are ordered, with pertinent findings that include a hemoglobin level of 11.1 g/dL (reference range, 13.5-17.5 g/dL) and a platelet count of 24 × 109/L (reference range, 136-436 × 109/L). A chemistry panel reveals the following: Sodium level: 134 mEq/L (134 mmol/L; reference range, 135-145 mEq/L) Potassium level: 3.2 mEq/L (3.2 mmol/L; reference range, 3.5-5 mEq/L) Creatinine level: 0.6 mg/dL (53.04 µmol/L; reference range, 0.7-1.2 mg/dL) Glucose level: 148 mg/dL (8.21 mmol/L; reference range, <140 mg/dL) Bilirubin level: 4.7 mg/dL (80.37 µmol/L; reference range, 0.3-1 mg/dL) Magnesium level: 1.3 mg/dL (0.53 mmol/L; reference range, 1.5-2.5 mg/dL) Ammonium level: 153.3 µg/dL (90 μmol/L; reference range, 11-79 µg/dL) Ionized calcium level: 3.96 mg/dL (0.99 mmol/L; reference range 4.6-5.6 mg/dL) His troponin level is 0.07 ng/mL (0.07 μg/L; reference range, <0.12 ng/mL). Serum alcohol testing results are negative, and a urine toxicology screen is negative for cannabinoids, cocaine, and opiates (note that methadone usage may not cause a positive opiate result). A CT scan of the brain is negative for acute abnormalities. The patient is initially thought to have had a seizure and is cautiously given benzodiazepines to prevent a recurrence. An electrocardiogram (ECG) is then performed (Figure 1). Soon afterwards, an abnormal tracing is seen on the cardiac monitor (Figure 2), and the patient becomes pulseless and apneic and requires cardiopulmonary resuscitation. Figure 1. Figure 2. Discussion The cardiac rhythm strip (Figure 2) demonstrated torsade de pointes (French for "twisting of the points"), otherwise known as simply "torsades" or polymorphic ventricular tachycardia. Figure 2. The initial ECG (Figure 1), which was obtained before the development of the torsades, revealed a prolonged QT interval and notched T waves. A prolonged QT interval is often noted incidentally on an ECG in an asymptomatic patient; however, in a patient who presents with palpitations, presyncope, syncope, or cardiac arrest, the presence of a prolonged QT interval should raise particular concern for torsade de pointes. Figure 1. QT prolongation can be either acquired or congenital. A thorough clinical history-taking and knowledge of the patient's current medications is very important for this differentiation. Congenital long QT syndrome (LQTS) is a disorder characterized by abnormal QT-interval prolongation on the ECG caused by cardiac myocyte ion channel gene mutations, with a propensity to ventricular tachyarrhythmias. Patients are typically young and may present with syncope or sudden death.[1,2,3,4] Acquired QT interval prolongation may be drug-induced, or it may be caused by certain electrolyte derangements, such as hypomagnesemia, hypokalemia, and hypocalcemia. Many drugs have been implicated, including class 1A antiarrhythmic drugs such as quinidine and procainamide and class III antiarrhythmics such as amiodarone and sotalol. Other drugs that have been implicated include antihistamines (terfenadine, astemizole), macrolide antibiotics (erythromycin, clarithromycin, clindamycin, azithromycin), pentamidine, serotonin receptor antagonists (ketanserin), diuretics (indapamide), certain fluoroquinolone antibiotics, tricyclic antidepressants, antipsychotics (phenothiazines, haloperidol, mesoridazine, pimozide, thioridazine, ziprasidone), gastrointestinal motility enhancers (cisapride, domperidone), inotropes (amrinone, milrinone), antimalarials (chloroquine, hydroxychloroquine), toxins (organophosphates, arsenic), protease inhibitors, and methadone.[1,5,6,7,8,9] Drug-induced prolongation of the QT interval is directly linked to a modification in myocardial cell repolarization, which is mediated by the efflux of potassium ions. The shape of the action potential depends on the balance between sodium and calcium inflow and potassium outflow. Two subtypes of the delayed rectifier K+ current, IKr (rapid) and IKs (slow), are responsible for repolarization. The human ether-a-go-go related gene ( hERG ; also termed KCNH2 ) codes for a protein known as the Kv 11.1 potassium ion channel, which mediates the repolarizing potassium current IKr. Blockage of the hERG -encoded potassium channels has been implicated as a cause of drug-induced QT prolongation. A strong correlation is noted between IKr blockade and ventricular arrhythmia or sudden death. Drugs that block the IKr channel increase the QT interval and allow inward current, particularly calcium, to reactivate, leading to early after-depolarizations in cardiac tissue that may result in torsades. Other drugs implicated in QT prolongation have no effect on the potassium channels; therefore, additional cardiac mechanisms can play a significant role.[2,5] Some medications prolong the QT interval at specific doses, whereas others may act at any dose. The patient's underlying decompensated hepatitis C virus liver cirrhosis is a significant predisposing factor for QT interval prolongation and the development of torsades.[4] Many medications that prolong the QT interval, including methadone, are metabolized by the hepatic cytochrome P450 3A4 (CYP3A4) system. Therefore, hepatic dysfunction can alter drug metabolism and increase plasma concentrations of QT-prolonging drugs, thereby contributing to QT prolongation. This risk is further exacerbated by potential drug-drug interactions involving CYP3A4 inhibitors. When administering a drug that potentially prolongs the QT interval, numerous predisposing factors for torsades development must be considered, including advanced age, obesity, poor nutrition (anorexia nervosa, starvation diets, alcoholism), bradycardia (<50 beats/min), cerebrovascular disease (intracranial and subarachnoid hemorrhage, stroke, intracranial trauma, thalamic hematoma), congenital long QT syndrome, heart failure (cardiomyopathy, dilated or hypertrophic), hypoglycemia, hypothermia, hypothyroidism, myocardial ischemia or infarction, organophosphate exposure, pheochromocytoma, pituitary insufficiency, coadministration of other QT prolonging agents, and hypoxia. If a drug-to-drug interaction is suspected, the drug should be withdrawn. Ehret and colleagues[9] studied a population of active or former intravenous drug abusers and suggested that methadone (even at low doses), CYP3A4 inhibitors, and hepatic dysfunction contributed to prolongation of QT. Methadone delays cardiac repolarization by blocking the flow of potassium ions through the hERG channels, but no evidence suggests interaction between this drug and nucleoside reverse transcriptase inhibitors.[5,7,9,10] Torsade de pointes is characterized by QRS complexes that vary in axis and amplitude over the isoelectric line ("twisting around the points," as the name implies). Other associated characteristics include the presence of long and short beat-to-beat (RR) interval onset after an early premature ventricular contraction. A relationship between the degree of QT interval prolongation and the development of torsades is noted. The QT interval varies directly with heart rate, and a correction is required in order to compensate for heart rate. A commonly used correction (QTc) is the Bazett correction (QTc=QT/√RR), wherein QT is the longest QT interval measured on the ECG, and RR is an average RR interval. QT measurement should be made manually from a 12-lead ECG, and it is calculated from the beginning of the QRS complex to the end of the T wave and averaged over three to five beats in a single lead. Prominent U waves should be included in the measurement if they merge into the T wave. It is advisable to assess QT during peak plasma concentration of any ingested QT-prolonging substances and to correct it for heart rate while looking for other warning signs, including the appearance of prominent U waves, extrasystoles, and U wave augmentation after extrasystole. Corrected QT is considered prolonged if it is beyond 440 msec for adult males, 460 msec for adult females, and 500 msec in the presence of ventricular depolarization abnormalities (ie, bundle branch blocks or intraventricular conduction delay greater than 120 msec). The uncorrected QT interval should also be considered, however, as a very long QT (>600 msec) after drug exposure is a marker of an increased risk for torsades.[1,5,11] The patient in this case was initially treated with 2 g of intravenous magnesium sulfate and 1 g of calcium chloride. Despite this, he developed recurrent torsade de pointes. He underwent repeated defibrillation followed by irregular rhythms, including premature atrial complexes and ventricular bigeminy. The recurrent episodes of torsade de pointes were then treated with an intravenous bolus of lidocaine followed by a 2-mg/min infusion. Normal sinus rhythm then returned, and the patient slowly improved and regained consciousness. In this case, the cause of the patient's QT prolongation was likely multifactorial and probably included the chronic use of methadone and electrolyte derangement. Slight hypomagnesemia, hypocalcemia, and hypokalemia were noted. These mild electrolyte abnormalities alone are not sufficient to result in torsade de pointes, as evidenced by the persistence of episodic torsade de pointes despite electrolyte replacement. Once the methadone was withdrawn, however, no further episodes of torsade de pointes occurred, and the QT interval normalized. Cirrhotic cardiomyopathy is often associated with QT interval prolongation and is an important consideration in the differential diagnosis of acquired QTc prolongation.[12,13] However, in this patient's case, the arrhythmogenic effect was more likely medication-related than a direct consequence of cirrhosis, given the resolution of QTc prolongation following methadone withdrawal. Treatment of Torsade de Pointes The immediate and primary treatment for torsades is intravenous magnesium sulfate, typically as a 2-g bolus followed by an infusion of 2-4 mg/min. This therapy is recommended regardless of the patient's serum magnesium levels.[3] Repeated doses may be needed, titrated to suppress ectopy and nonsustained ventricular tachycardia episodes while precipitating factors are corrected.[3] Magnesium is not contraindicated in liver disease, although caution may be necessary in severe renal failure. For patients experiencing hemodynamically unstable torsades, or if the arrhythmia persists or degenerates into ventricular fibrillation (VF), immediate unsynchronized defibrillation (direct current cardioversion) is indicated.[3,4] Correction of electrolyte abnormalities is crucial. Serum potassium levels should be maintained in the high-normal range (4.5-5 mmol/L).[3,4] Hypokalemia and hypomagnesemia are recognized factors that can trigger ventricular arrhythmias, including torsades. If both magnesium and potassium levels are low, magnesium should be repleted first to facilitate potassium replacement. For recurrent torsades, particularly in patients with acquired long QT syndrome and bradycardia that is refractory to magnesium, rate-increasing therapies are recommended to shorten the QT interval and prevent recurrences. These therapies include the following: Overdrive transvenous pacing: Pacing with a slightly higher rate than the baseline rhythm can temporarily suppress slow recurrent or incessant VT. Isoproterenol infusion: Isoproterenol works by increasing heart rate and abolishing the post-extrasystolic pauses that can precipitate torsades. However, it is contraindicated in patients with congenital long QT syndrome and ischemic heart disease.[3,4] Maintaining a heart rate greater than 70 beats/min protects against drug-induced torsades.[2,3,4] Any offending QT-prolonging medications should be discontinued whenever drug-induced arrhythmias are suspected. Medications such as amiodarone and procainamide, which prolong the QT interval, should not be used for torsades or arrhythmic storm associated with a prolonged QT, as they can worsen the condition.[2,3] Patients who require a potentially arrhythmia-inducing drug should undergo regular ECG and other tests based on their profile and the drug's characteristics.[4] While not a first-line approach to acutely terminate torsades, beta-blockade is a component of the multifaceted approach to managing arrhythmic storm (which can include torsades).[2] Nonselective beta-blockers (eg, propranolol) are preferred and often used in combination with intravenous amiodarone in patients with structural heart disease (SHD) and electrical storm, unless contraindicated.[2,3,4] Lidocaine, a class IB antiarrhythmic, blocks fast inward sodium currents and can slightly shorten the QTc interval. It is included in some guidelines for torsades and electrical storm management and is considered beneficial for 4 cardiac arrest due to shock-refractory VF or polymorphic VT.[3,4] It may be considered if beta-blockers and amiodarone are ineffective.[4] Long-term management and prevention of sudden cardiac death in patients susceptible to torsades and other ventricular arrhythmias primarily involves implantable cardioverter-defibrillators (ICDs) and comprehensive medical strategies.[2,3,4] This case illustrates an incident of likely drug-induced torsade de pointes resulting from methadone usage in the setting of electrolyte abnormalities. The case highlights the need for an evaluation for potential cardiogenic causes of syncope in patients who present with an abnormal ECG. Acquired QT interval prolongation may be drug-induced, or it may be caused by certain electrolyte derangements, such as hypomagnesemia, hypokalemia, and hypocalcemia. Many drugs have been implicated, including class 1A antiarrhythmic drugs such as quinidine and procainamide and class III antiarrhythmics such as amiodarone and sotalol. Other drugs that have been implicated include antihistamines (terfenadine, astemizole), macrolide antibiotics (erythromycin, clarithromycin, azithromycin, clindamycin), pentamidine, serotonin receptor antagonists (ketanserin), diuretics (indapamide), certain fluoroquinolone antibiotics, tricyclic antidepressants, antipsychotics (phenothiazines, haloperidol, mesoridazine, pimozide, thioridazine, ziprasidone), gastrointestinal motility enhancers (cisapride, domperidone), inotropes (amrinone, milrinone), antimalarials (chloroquine, hydroxychloroquine), toxins (organophosphates, arsenic), protease inhibitors, and methadone. Immediate treatment for patients who develop torsades can be categorized into pharmacologic and nonpharmacologic approaches. Intravenous magnesium sulfate (2-g bolus followed by an infusion of 2-4 mg/min) is the initial therapy, regardless of the serum levels of magnesium.
The Sun
04-07-2025
- Health
- The Sun
Woman died after ‘rampant STI' invaded her body and attacked her vital organs – 4 signs you must know
A WOMAN died after an untreated STI invaded her body and attacked her vital organs. The unnamed woman from Alaska, who was in her 50s, passed away from disseminated gonococcal infection (DGI). 1 This is a rare but serious complication of the sexually transmitted infection gonorrhoea. It occurs when Neisseria gonorrhoeae bacteria spreads from the initial site of infection, seeping into the bloodstream and vital organs. DGI is thought to occur in just 0.5 percent of all gonorrhoea cases. The woman arrived at her local emergency department in Anchorage, Alaska, in spring this year, already in a critical condition. She was in respiratory distress - when the lungs aren't working properly due to serious illness - and was diagnosed with septic shock and heart failure, caused by endocarditis, a potentially fatal infection of the heart's inner lining. Further testing revealed her body had been invaded by gonorrhoea bacteria. But the patient wasn't diagnosed with DGI until after she'd passed away. There were no records of her being tested for gonorrhoea prior to her presenting at the emergency department. She'd been treated twice in the prior six months for opioid abuse, according to the Alaska Department of Health. Eight cases of DGI were reported in Alaska between January and May 2025, report authors added. How to put a condom on - NHS The cases were spotted after patients were evaluated in emergency departments in Anchorage. Epidemiologic investigations didn't establish connections between any of the DGI cases. While gonorrhoea can be got rid of with antibiotics, some infected people may not get tested or treated as they don't have symptoms of the STI, according to Dr Liz Ohlsen, a staff physician with the Alaska Department of Health who wrote the report. As a result, they run the risk of developing dangerous DGI, she told the Alaska Beacon. Health officials fear that a strain less likely to cause symptoms is circulating in Alaska, Dr Ohlsen went on. 'We think the most likely explanation for the rise in DGI cases is that more people with gonorrhoea are not getting tested and treated in a timely manner," she said. "Asymptomatic infections are thought to pose a greater risk of persistent untreated infection because people are less likely to have sought care." The Alaska Department of Health bulletin warned that people in Anchorage with a new sexual partner, more than one sexual partner, or a partner with multiple partners might be at risk of acquiring a strain of N. gonorrhoeae that's thought to carry a higher risk of causing DGI. Symptoms of gonorrhoea Typical symptoms of gonorrhoea include: A thick green or yellow discharge from the vagina or penis Pain when urinating Pain and discomfort in the rectum Lower abdominal pain and bleeding between periods in women and other people with a uterus or ovaries Gonorrhoea can affect other parts of your body that come into contact with semen or vaginal fluid. This can cause: Pain, itching and discharge from your bottom A sore throat Eye redness, pain and discharge However, many people infected with gonorrhoea will have no symptoms, especially for infections in the throat, vagina or rectum. This lack of symptoms makes it important to test regularly when having sex with new or casual partners. If you do get symptoms, they usually start around two weeks after infection, although they sometimes do not appear until many months later. Untreated gonorrhoea can lead to serious health complications including: Infertility and pelvic inflammatory disease (PID) An infection of the female reproductive system, which includes the womb, fallopian tubes and ovaries An infection in the testicles or prostate In rare cases, gonorrhoea bacteria can cause a disseminated gonococcal infection (DGI). It can cause frequently results in purple or pus-filled spots on the skin, joint pain, inflamed tendons or septic joint infections. Rarely, DGI can lead to inflammation of the liver, endocarditis - an infection of the inner heart lining - and meningitis. Having gonorrhoea during pregnancy can increase your risk of premature birth and your baby having a low birth weight. There's also a risk the infection could spread to your baby's eyes during birth, which is called gonococcal conjunctivitis. This can cause blindness if it's not treated with antibiotics. "While no specific sexual network has been identified, this strain may be circulating more broadly among persons with gonorrhea infection in Southcentral Alaska," report authors said. "The absence of documented gonorrhoea risk factors in most DGI cases suggests patients may not be asked about or disclosing key sexual history. "Few had symptoms before presenting with DGI, consistent with its progression from untreated mucosal infections. "Asymptomatic or mildly symptomatic patients with GC are less likely to seek health care and may be at a higher risk of persistent untreated infection leading to disseminated infection." In the UK, health officials issued warnings earlier this year over cases of "extensively drug resistant" gonorrhoea that aren't responding to antibiotic treatment. While most gonorrhoea infections can be treated effectively, certain resistant strains "present significant treatment challenges", the UK Health Security Agency (UKHSA) said. It warned that increased resistance could one day make the STI 'untreatable'. Meanwhile, the NHS announced it would begin vaccinating people against gonorrhoea come August, after cases of the STI hit a record 85,000 in 2023. Local sexual health clinics will offer the jab to gay and bisexual men, who are most at risk. Patients will receive the 4CMenB vaccine for meningitis B, which has been found to nearly halve the chances of catching gonorrhoea in adults. Health chiefs reckon they can prevent around 10,000 cases per year.
CBC
29-06-2025
- Health
- CBC
Saskatoon City Hospital increases hours for emergency department
The Saskatoon City Hospital is increasing the hours of operation for its emergency department from 9:00 a.m. to 6:00 p.m. The new schedule begins June 29. It follows several months of reduced hours at the emergency department, which was only operational from 9:00 a.m. to 4:00 p.m. The hospital says the hours have expanded because the Saskatchewan Health Authority (SHA) has made progress in stabilizing physician staffing, and is now taking a "phased approach" to resuming full-time hours. The introduction of 109 new acute care beds at the hospital is also still underway. The initiative, funded by an SHA infusion of $15 million, began in March 2025 and is expected to take 12 to 16 months. Understaffing has been a persistent issue at Saskatoon hospitals. On New Year's Eve 2024, the emergency department temporarily reduced its hours to just 5 p.m. to 8:30 p.m., saying some of its doctors were sick. In May 2025, emergency room patients at the Royal University Hospital and St. Paul's Hospital were forced to be treated in hallways and waiting rooms due to lack of available space. Alongside the increased hours at the Saskatoon City Hospital, the emergency departments at the Royal University Hospital and St Paul's Hospital remain open to the public 24 hours a day, seven days a week.
Yahoo
29-06-2025
- Health
- Yahoo
Saskatoon City Hospital increases hours for emergency department
The Saskatoon City Hospital is increasing the hours of operation for its emergency department from 9:00 a.m. to 6:00 p.m. The new schedule begins June 29. It follows several months of reduced hours at the emergency department, which was only operational from 9:00 a.m. to 4:00 p.m. The hospital says the hours have expanded because the Saskatchewan Health Authority (SHA) has made progress in stabilizing physician staffing, and is now taking a "phased approach" to resuming full-time hours. The introduction of 109 new acute care beds at the hospital is also still underway. The initiative, funded by an SHA infusion of $15 million, began in March 2025 and is expected to take 12 to 16 months. Understaffing has been a persistent issue at Saskatoon hospitals. On New Year's Eve 2024, the emergency department temporarily reduced its hours to just 5 p.m. to 8:30 p.m., saying some of its doctors were sick. In May 2025, emergency room patients at the Royal University Hospital and St. Paul's Hospital were forced to be treated in hallways and waiting rooms due to lack of available space. Alongside the increased hours at the Saskatoon City Hospital, the emergency departments at the Royal University Hospital and St Paul's Hospital remain open to the public 24 hours a day, seven days a week.
ABC News
26-06-2025
- Health
- ABC News
Hospital study finds link between La Niña events and spread of deadly Vibrio vulnificus infection
Anamika Ganju had not seen anything like it in more than 20 years as an intensive care clinician. Two men in three days had presented to the emergency department with baffling similarities. Both men, aged around 80, had cuts that had rapidly progressed to grotesque infections, with their skin sloughing away to reveal gaping wounds. Both had been crabbing in the muddy estuaries of rivers swollen by floodwater that had devastated the Wide Bay region just weeks before. And to the despair of Dr Ganju and her colleagues, both men were unresponsive to the standard antibiotics used to treat bacterial infections. "It is pretty devastating," Dr Ganju said. "You're like, 'Why is this patient so sick? What am I missing? He shouldn't be so sick … with [the] signs and symptoms I'm seeing, they should start getting better." Analysis of decaying tissue from one of the patients in March 2022 showed it was teeming with Vibrio vulnificus — a flesh-eating bacteria rare enough in the tropical north of Queensland, but almost unheard of in the Fraser Coast region about three hours' drive north of Brisbane. Vibrio vulnificus was known to thrive on the additional nutrients brought by floodwaters, but Dr Ganju said the scarcity of the infection in the hospital's sub-tropical location meant it was not initially considered a likely diagnosis. "To be honest, in my career — I've been doing this for 25 years — I had not seen a Vibrio [case] before this," Dr Ganju said. The medical team pivoted to use ciprofloxacin, an antibiotic known to target Vibrio vulnificus, and both patients underwent operations to remove and replace the decaying flesh. Three more fishermen presented to the hospital with bacterial infections over the next six months and, by then, the team was on high alert. Source: Queensland Health "We would always ask whether there was exposure to … marine water or were they in a boat, and if we got that history we would start the ciprofloxacin [immediately]," Dr Ganju said. More than one in four patients can die once the infection takes hold, but all five men survived. The third patient, Hervey Bay fisherman Rodney Drier, required 18 operations and after contracting a fungal infection had his left hand amputated. He rues the slip of a knife while cutting up a catfish to use as crab bait which had life-changing consequences. "It ruined my lifestyle … took my life away from me," the disability pensioner said. Once all patients were discharged in 2022, Dr Ganju and her colleagues recorded their experience in a clinical case report published today in the Rural and Remote Health Journal. By analysing the frequency of Vibrio vulnificus infections in Queensland, lead author and senior pharmacist Daniel Bermingham found spikes of infections over the past 25 years corresponded with La Niña weather events. While there were only 86 cases of Vibrio vulnificus infections in Queensland between 1998 and 2023, the number of cases increased nearly fivefold during a La Niña event. With carbon emissions known to contribute to more frequent and extreme La Niña events, Mr Bermingham said his research showed climate change increased the risk of Vibrio vulnificus infections. The researchers hope the findings will result in a public awareness campaign of the potentially fatal risks and best practice if the infection is acquired. "The first aid care that you can provide to yourself … is to get the first aid kit out, give [the wound] a good wash and make sure that you can clean the wound from injury," Mr Bermingham said. "Get some chlorhexidine or some betadine and put it onto the actual wound and go see the GP or ED if it does tend to get worse." Allen Cheng, the director of Monash Infectious Diseases at Monash Health in Victoria, was not involved in the clinical case report and does not believe "major changes" to public health messaging are warranted. However, he agreed the epidemiology, or distribution, of Vibrio vulnificus was becoming more common in subtropical regions due to global warming. "The case report … is at least a very good reminder to physicians that this [infection] does exist and we may be seeing changes in the epidemiology." In a statement, Queensland Health says the department issues public health advice about the risks of exposure to floodwaters, particularly around severe weather events. The Queensland Health guidelines prescribing antibiotics in cases of severe infections were last reviewed in 2024, the spokesperson said. The guidelines now advise using ciprofloxacin — the antibiotic targeting Vibrio vulnificus — if the patient is exposed to water, including in subtropical regions like Hervey Bay. As he tends to his orchids, Mr Drier is emphatic that there needs to be improved public awareness of the infection. "Especially when you see people walking in floodwaters in the streets," he said. "I think, 'You stupid fools, if only you knew'. One scratch and you've got a bug."
