Latest news with #patient
Medscape
2 hours ago
- General
- Medscape
Medical Misogyny or Following the Differential Dx?
I recently presented a clinical scenario of a young woman who presented with fatigue and had a long history of nightmares. I was concerned that she might have posttraumatic stress disorder (PTSD), and I asked readers whether they agreed with my management of this patient. Thank you for the comments on this case. The majority of the comments focused on a workup for the patient's symptoms beyond mental illness, which is completely appropriate for this patient. First, a targeted history should be completed to include the following elements: Menstrual history to evaluate the possibility of anemia due to irregular menses and pregnancy Cold intolerance or skin and hair changes, as a potential sign of hypothyroidism Any alterations in appetite and diet, which could indicate disordered eating and/or a possible vitamin deficiency Medication use, including supplements Substance use I would also recommend the following basic laboratory evaluation: Other labs may be ordered, as needed, based on the patient's targeted history. But adding all those elements to this case would yield quite a lengthy document to read online! And of course, there are always more questions to ask of patients and more studies to be ordered, but the pressure of time in primary care dictates that we be judicious with our fact-gathering. Although my decision to ask the patient about past events that might relate to her fatigue and bad dreams was the most popular answer selected in the reader poll, some commenters disagreed with my approach. I was surprised by multiple comments that suggested my consideration of a potential psychological disorder would be considered patronizing or offensive to this patient, and one commenter recommended 'physiology before psychiatry.' I respectfully disagree. First, a mental health or sleep disorder is at the top of the differential diagnosis of an otherwise healthy young woman with fatigue. When a physician fails to address a potential mental health disorder for fear of offending said patient, they risk delayed diagnosis, worsening symptoms, diminished treatment options, and a breakdown of trust in her care, all of which could have devastating consequences. As mentioned in my original article, PTSD negatively affects multiple domains of function and is associated with an increased risk for suicide. I completely understand that patients can feel marginalized by the idea of a mental health diagnosis. And it's entirely understandable that a woman presenting with persistent fatigue might fear that a psychological explanation simply repeats historical patterns of medical sexism; after all, attributing women's health complaints to 'hysteria' is a real historical wrong. Yet when that same fatigue is coupled with a decade-long history of recurring nightmares — symptoms strongly suggestive of an underlying mood or stress ‐ related disorder — a thoughtful clinician must expand the differential diagnosis to include those possibilities. By transparently describing how each symptom fits into a broader clinical picture, the doctor honors the patient's concerns and makes a diagnosis based on comprehensive evidence, not gender bias. In responsible practice, a physician uses validated screening questions, explains the medical rationale clearly, and invites open dialogue with the patient (at their own pace). That way, mental health issues are assessed objectively, based on clinical need and symptom presentation. We, as a society, need to move away from stigmatizing mental health diagnoses, and that starts with the patient encounters we have every day. There is no reason that mental health diagnoses should be placed at some level below other diagnoses. Mental health diagnoses incur significant amounts of morbidity and are risk factors for other diseases, such as coronary heart disease. Patients who are diagnosed with mental health disorders should not feel any different from patients with a diagnosis of type 2 diabetes or rheumatoid arthritis. It is up to us, as clinicians, to lead insightful, evidence-based, empathic evaluations of our patients to accurately diagnose their conditions and treat them appropriately. I hope that this case reminds you of that calling.
Medscape
15 hours ago
- Health
- Medscape
A 53-Year-Old Woman With Sudden-Onset Dysphonia and Paresis
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. A 53-year-old woman comes to the emergency department (ED) in the middle of the night with a 1-day history of diffuse, constant, and worsening abdominal pain. The pain is not associated with fever, nausea, vomiting, constipation, diarrhea, or urinary symptoms. Her review of symptoms is positive only for visual blurriness and xerostomia. The patient takes atorvastatin and atenolol/chlorthalidone. She has no recent history of trauma or hospitalization. Past surgeries include an appendectomy at age 10 years and a hysterectomy at age 42 years. She lives with her husband and adult son. When asked about possible contributory environmental or vocational exposures, she states they all work from home selling homemade crafts and jewelry online and at regional festivals. She adds that they have recently taken workshops on fruit and vegetable canning and ornamental fish aquaculture to expand their business. Her husband and son are not ill, although they have generally shared the same environment and food. Physical Examination and Workup The patient's initial vital signs in the ED include a temperature of 98.6 °F, heart rate of 102 beats/min with sinus tachycardia, blood pressure of 116/50 mm Hg, and respiration rate of 18 breaths/min. Her oxygen saturation level is 99% on room air. Her Glasgow Coma Scale score is 15. She rates her level of pain at 7 out of 10. Once the patient is undressed and placed in a gown, a physical examination is performed. The results are normal except for a mildly distended abdomen with voluntary guarding along the lower quadrants. No rebound tenderness is noted. Her mucous membranes are slightly dry. The results of the neurologic examination are grossly intact. An intravenous (IV) line is inserted, and blood is drawn for laboratory studies. The results of a CBC count, comprehensive metabolic panel, and urinalysis are normal. Plain abdominal radiography reveals distended loops of bowel and air-fluid levels. Similar radiographic findings from a different patient are shown below (Figure 1). Figure 1. An abdominal CT scan with IV contrast confirms the dilated loops of small bowel but reveals no evidence of a mechanical obstruction. Figure 2 shows an example of an intestinal obstruction on a CT scan in a different patient. Figure 2. Intestinal obstruction. Color-enhanced coronal CT scan. After a consultation finds no evidence of an acute abdomen requiring surgery, the patient is sent to the ED observation unit for placement of a nasogastric tube, IV hydration, analgesia, and monitoring. Over the course of 4-5 hours in the observation unit, the patient develops diplopia and her speech becomes less intelligible. She also reports dyspnea. Her temperature is 98.2 °F, heart rate 52 beats/min, blood pressure 92/52 mm Hg, and respiration rate 28 breaths/min. Her oxygen saturation level is 97% on room air. Her Glasgow Coma Scale score is 14-15. She rates the level of her pain at 2 out of 10. The physician on duty is unable to see the patient immediately and orders a CT scan of the brain, repeated blood tests, and arterial blood gas analysis. The results of the brain CT scan are normal. The arterial blood gas analysis demonstrates moderate respiratory acidosis. The findings are: Arterial blood pH: 7.32 (reference range, 7.35-7.45) Partial pressure of oxygen (PO 2 ): 94 mm Hg (reference range, 75-100 mm Hg) ): 94 mm Hg (reference range, 75-100 mm Hg) Partial pressure of carbon dioxide (PCO 2 ): 56 mm Hg (reference range, 35-45 mm Hg) When the physician returns to see the patient, he notes bilateral ptosis, dysphonia, dysarthria, and bilateral cranial nerve VI paresis. Discussion Tolosa-Hunt syndrome is a granulomatous inflammatory process near the cavernous sinus or within certain areas of the orbits. The disease manifests with one or more episodes of unilateral ocular pain in addition to paralysis of cranial nerves III, IV, and/or VI. In contrast to this patient's presentation, there is typically no gastrointestinal prodrome or progression of the neurologic manifestations beyond the ocular nerves. Symptoms of lead toxicity can include anorexia, constipation, abdominal pain, nausea, and vomiting; other features may include renal dysfunction and neurological symptoms.[1] This patient's gastrointestinal symptoms did not include nausea, vomiting, or constipation; her comprehensive metabolic panel was within normal limits; and her neurological function was grossly intact. In North America, tick paralysis is common during the spring and summer when ticks are most active. When this patient was undressed and placed in a gown in the ED, a tick would likely have been discovered. The neurologic manifestations occur while the tick is attached. Once the tick is removed, the paralysis resolves. The prodrome is an influenzalike illness, and acute abdominal pain is not a typical presentation. The second stage is an ascending paralysis, not a descending paralysis. Patients are ataxic and exhibit lower extremity muscular weakness. Notably, however, tick paralysis can cause diplopia, difficulty swallowing, and speaking, as in this case, highlighting that it is an important item on the differential diagnosis. Botulism is a neuromuscular disease caused by toxins generated by the anaerobic, gram-positive bacterium Clostridium botulinum (Figure 3). Six syndromes are recognized: infant, foodborne, wound, adult colonization, inhalational, and iatrogenic. Of the eight neurotoxins (A to H), toxins A, B, and E (F, rarely) affect humans; types C and D are associated with disease in animals.[2,3] Type H was discovered in 2013.[4] Botulinum neurotoxins are considered the most potent biologic poison known.[2,3] Figure 3. Color-enhanced image of Clostridium botulinum bacteria (botulism bacillus). Of the eight C botulinum toxins (A to H), the ones that are likely to be poisonous to humans are A, B, and E, and rarely F. Type A produces the most severe syndromes. Type E is usually associated with botulism caused by consumption of aquatic food. Neurotoxin H was the last one discovered in 2013.[2] Condition Overview From 2011 to 2015, 162 cases of botulism were reported annually (mean)[3]; infant botulism, foodborne botulism, and wound botulism occurred in 71%-88%, 1%-20%, and 5%-10% of these cases, respectively. For foodborne botulism, the incubation period from first exposure to symptom onset can be from 12 to 72 hours (range, 2 hours to 8 days). The classic manifestations begin with a symmetrical paresis or paralysis starting from head to toe. The initial symptoms of botulism poisoning include ptosis, dysphonia, dysphagia, dysarthria, xerostomia, and visual difficulties (ie, bulbar manifestations).[2,3] Although death was a frequent outcome in the past, it rarely occurs today. Before 1950 or so, foodborne botulism carried a mortality rate of 60%-70%. That rate dropped to 3% for all the different types of botulism between 1975 and 2009.[3] Two principal causes of early death are complete airway obstruction from a food bolus as the muscles of deglutition become paralyzed and respiratory failure with paralysis of the diaphragm and intercostal muscles.[2] Once introduced into the body, the toxin enters the neuronal cells at the voluntary motor and autonomic neuromuscular junctions. There, it disrupts the release of neurotransmitter (acetylcholine) across the junction. With acetylcholine transmission blocked, the receptor sites of the motor and autonomic cells lie vacant. Flaccid paralysis occurs.[2,3] This process cannot be reversed. It may take months for the regeneration of the neurotransmitter mechanics.[2] The initial manifestations of botulism may be misleading. A patient who presents at the early stage may be alert and afebrile. The patient may sense the minute anatomic changes, but these subjective concerns are subtle and may be attributed to more typical maladies. Common misdiagnoses at this stage include alcohol or drug intoxication and psychiatric disorders.[2] Later, the neurologic signs become dominant, and botulism may be misdiagnosed as stroke, Tolosa-Hunt syndrome, meningitis, myasthenia gravis, tick paralysis, or Guillain-Barré syndrome, among other conditions.[1,2,5-7] Rarely, the gastrointestinal manifestations of botulism may predate or obscure the classic neurologic symptoms.[2,3] Botulism has been mistaken for acute bowel obstruction.[8,9] It is not until the neurologic manifestations come to the forefront that the correct diagnosis is made. In the patient in this case, the early ptosis was mistaken for lack of sleep and the xerostomia for dehydration. Nevertheless, the workup for a bowel obstruction (ie, abdominal radiographs and a CT scan of the abdomen with contrast) was reasonable because it is a more common disorder. In-depth questioning of this patient revealed that several days before she came to the ED, she opened and tasted a batch of canned jalapeño peppers she had made a few months earlier. She was planning to take them to a parish food drive. Her husband and son did not consume any of the peppers. With blockade of acetylcholine transmission, motor and autonomic cells lie vacant, leading to flaccid paralysis; this process cannot be reversed and regeneration of neurotransmitter mechanics may take months. Only rarely do the gastrointestinal manifestations of botulism predate or obscure the classic neurologic symptoms, but this has resulted in botulism being mistaken for acute bowel obstruction. Botulism is characterized by symmetrical paresis or paralysis starting from head to toe (descending paralysis). Reporting Responsibilities and Treatment Once botulism is included in the differential diagnosis, three actions must occur. First, the patient's status must be NPO to prevent aspiration; nasogastric tube feeding or total parenteral nutrition can be considered in cases with severe ileus. Second, assessment of respiratory capabilities is critical. It can be accomplished through various measurements, such as negative inspiratory force, vital capacity, blood gas analysis, or capnography.[1,2] Carbon dioxide retention requires immediate consideration of aggressive airway management to counter respiratory paralysis and cardiorespiratory arrest. Third, the local public health department and the Centers for Disease Control and Prevention (CDC) must be notified. Any case of botulism in a community is a public health emergency. An urgent epidemiologic investigation must begin to search for additional cases and the source of the outbreak (eg, restaurants).[2] Electrodiagnostic studies may be used to evaluate muscle weakness.[2] Laboratory studies to confirm botulism include testing for neurotoxin in the serum, stool, and gastric juices; identifying clostridia in stool or wound cultures; and investigating the suspected sources of the toxin release. The mouse bioassay remains the criterion standard. Real-time polymerase chain reaction and mass spectrometry are also helpful.[2] However, waiting for the results of these studies cannot delay communication with the CDC once botulism is suspected. The CDC has the responsibility for releasing Botulinum Antitoxin Heptavalent (A, B, C, D, E, F, G) (Equine) (BAT). It is free and is available to clinicians 24 hours a day, 7 days a week.[2] Early administration of the antitoxin is associated with fewer days in the hospital and intensive care unit and a reduced need for mechanical ventilation support.[2,10,11] BAT neutralizes only the toxin circulating in the bloodstream that has yet to be incorporated into the cells.[1] In 2015, at a botulism mass casualty incident at a potluck meal in Lancaster, Ohio, the antitoxin was requested at 10 AM but did not arrive until midnight.[12,13] Therefore, the CDC should be contacted expeditiously. Note that Botulism Immune Globulin Intravenous (Human) (BIG-IV) (BabyBIG), the specific immunoglobulin G for infants with botulism who are younger than 1 year, is requested through the California Department of Public Health Infant Botulism Treatment and Prevention Program.[2,14] The patient in this case received the botulinum antitoxin, and her clinical manifestations resolved almost completely within 24 hours. She did not need intubation or mechanical ventilation support. BabyBIG is an orphan drug that consists of human-derived anti–botulism toxin antibodies. It has been approved by the US Food and Drug Administration for the treatment of infant botulism types A and B in infants younger than 1 year. The treating physician can obtain BabyBIG by contacting the California Department of Public Health's Infant Botulism Treatment and Prevention Program. It has been administered to more than 1500 infants with botulism and, compared with control patients, resulted in a 3.5-week decrease in length of hospitalization.[10,14] Proactive Strategies Any patient with a presumptive diagnosis of botulism may require invasive airway management, owing to impending paralysis. Patients who may have a difficult airway should be identified early. Such patients include those who have short necks, obvious nuchal and/or facial abnormalities, or disconcerting results on an airway assessment tool (eg, the Mallampati score). For this type of patient, elective intubation is safer than emergency intubation. Another situation that must be planned for is a community-wide outbreak with limited healthcare resources. Between 1977 and 2015, there were six foodborne botulism outbreaks involving multiple patients. The smallest outbreak (16 people) occurred in Texas in 2001 and was caused by contaminated chili at a church function. The highest caseload was 58 patients in Michigan in 1977. In this outbreak, home-canned peppers served at a local restaurant contained the botulinum toxin (Figure 4).[12] Figure 4. The mouse bioassay remains the criterion standard. Real-time polymerase chain reaction and mass spectrometry are also helpful, but these methods are not widely available and generally are limited to the CDC and reference laboratories. Important to note is that awaiting the results of these studies should not delay communication with the CDC once botulism is suspected. Stool culture is considered the criterion standard for confirming conditions such as Escherichia coli (Shiga toxin) infection and salmonellosis. Outbreak Strategies As patients involved in an outbreak arrive at an ED, there may be a paucity of respiratory therapists and equipment to evaluate progressive respiratory failure expediently. One solution is the single-breath counting test (SBCT).[15] It is useful because its functionality is not limited by skill set, equipment needs, or geography. To perform the SBCT, the clinician asks the patient to sit upright, take a deep breath, and then begin counting upward at a rate of two numbers per second in their normal speaking voice; they should continue as long as possible while exhaling.[2] Studies involving myasthenia gravis indicate that the SBCT has a moderate correlation to forced vital capacity and that reaching 25 or higher is indicative of normal respiratory muscle function.[2] The next step is to triage certain patients to outlying institutions to avoid compromising healthcare capabilities at the initial hospital. Reverse triage may be the safest method — that is, transporting the intubated patients whose condition is less likely to deteriorate en route. Botulism is a complicated disease for both patients and their communities. It must be managed with equal measures of skill and flexibility.
Medscape
2 days ago
- General
- Medscape
Woman With Dysphagia, Regurgitation, and Throat Burning
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 and Initial Presentation A 56-year-old woman presents to the clinic with a 6-month history of intermittent dysphagia, primarily with solid foods, describing a sensation of "something stuck in her throat," along with a burning sensation in the throat and esophagus. She denies difficulty swallowing liquids. Her symptoms have remained relatively stable without significant progression over time. She also experiences gagging, coughing, nocturnal regurgitation, and congestion. She has a history of acid reflux that was treated with a proton pump inhibitor, which she is no longer taking. She takes antacids intermittently with minimal relief. She has a history of congenital hiatal hernia, which was repaired at age 11 years. She denies any fever, chills, chest pain, shortness of breath, abdominal pain, unintentional weight loss, hemoptysis, nausea, vomiting, or blood per rectum. On physical exam, the patient's abdomen was soft, non-tender, and non-distended. Her head, eye, ear, nose, and throat exams were also unremarkable, without a palpable neck mass. The rest of the physical exam was unremarkable. Basic labs were ordered, and the results, including thyroid function panel, were within normal limits. Workup Results The patient was prescribed a proton pump inhibitor and referred to a gastroenterologist. Given her persistent reflux symptoms without improvement despite anti-reflux medication, she was sent for esophagogastroduodenoscopy (EGD) to help stage her severity of reflux, to assess for laryngopharyngeal reflux, and to look for underlying structural abnormalities, such as recurrence of hiatal hernia. EGD also helps to evaluate for other potential, although less likely conditions, such as reflux esophagitis, Barrett's esophagus, or esophageal cancer. While ECG may be helpful to evaluate for potential atypical presentation of cardiac causes for her symptoms, it is unlikely given her lack of risk factors such as diabetes or history of cardiac disease. Chest x-ray assesses lung disease and bony structures but is unlikely to provide the anatomical detail required to provide any useful information. Esophageal manometry is useful for assessing for motility disorders and is generally used for esophageal symptoms not diagnosed on EGD or for patients undergoing anti-reflux surgery. EGD revealed mild gastritis without recurrence of hiatal hernia. Biopsies were negative. There was also no sign of laryngopharyngeal reflux, with no presence of pooling or residual material in the hypopharynx. Manometry was offered to the patient, but she opted for additional imaging. To better assess other anatomical factors extrinsic to the gastrointestinal tract that may be causing the patient's symptoms, she underwent neck ultrasonography, which revealed a small right thyroid nodule (0.7 cm X 0.5 cm X 0.8 cm) without any concerning features. She then underwent neck CT, which demonstrated an aberrant right subclavian artery originating from the aortic arch distal to the origin of the left subclavian artery, passing posterior to the esophagus while coursing toward the right. In addition, there is a fusiform aneurysmal dilatation of this aberrant right subclavian artery proximally, measuring approximately 1.6 cm in diameter, compared with a diameter of 0.6 cm more distally along the right subclavian artery (Figure 1). Figure 1. Neck CT showing aberrant right subclavian artery. The CT also demonstrated the sub-centimeter enhancing soft-tissue nodule within the right thyroid gland. No other pathologically enlarged or abnormally enhancing cervical lymph nodes were evident. Discussion Dysphagia lusoria is a rare condition caused by compression of the esophagus by an aberrant retroesophageal right subclavian artery. The right subclavian artery normally takes off as a branch of the brachiocephalic trunk, the most proximal great vessel of the aortic arch. Aberrant right subclavian artery (ARSA), however, takes off distal to the left subclavian artery, which is the most distal branch in a normal aortic anatomy. ARSA is the most common aortic arch anomaly, with a reported prevalence of 0.7%-2.0%.[1] It is caused by the involution of the right fourth vascular arch and proximal right dorsal aorta and the persistence of the seventh intersegmental artery originating from the proximal descending thoracic aorta.[2] Esophageal cancer is unlikely, as no masses were found on EGD. Dysphagia megalatriensis is also unlikely because she has no history or clinical signs of cardiac disease (eg, mitral valve pathology or atrial fibrillation). Zenker diverticulum, or a weakening of mucosa and submucosa in the upper esophagus, can present with globus sensation or dysphagia but also generally presents with halitosis and is usually a disease of the 7th or 8th decade of life. Neither ultrasound nor CT demonstrated this anatomical pathology. Thyroid goiter causing compressive symptoms is usually of significant size and can be appreciated on exam. The clinical presentation of dysphagia lusoria has significant heterogeneity. The most common symptoms are dysphagia, dyspnea, and chest pain.[3,4] It is more common in women than in men, with the mean age of symptom onset at 49.9 ± 19.4 years.[2] It is frequently associated with a Kommerell diverticulum, a dilation at the origin of the aberrant artery. The diverticulum results from failed regression of the previously mentioned fourth dorsal arch. The natural history of Kommerell diverticulum is unknown owing to the rarity of the condition, but both dissection and ruptures have been reported. In summary, dysphagia lusoria results from compression of esophagus by the retroesophageal aberrant right subclavian artery, which is an anatomical variant. Surgical intervention is generally indicated for patients with compressive symptoms. In asymptomatic patients, there is no established indication for repair. Some have proposed repair if the diverticulum reaches a certain size, with surveillance in asymptomatic cases. Some groups recommend surgical repair in all encountered cases of Kommerell diverticulum owing to a high rupture and dissection rate. In a single-center study of 45 patients, the average growth of Kommerell diverticulum was 1.45 ± 0.39 mm/year, with hypertension being the single statistically significant factor promoting growth.[5] The reported rupture and/or dissection rate at first encounter ranges broadly, from 0% to 50%.[1] A contained rupture of Kommerell diverticulum would lead to aortic hematoma. There are no known associations between Kommerell diverticulum and esophageal cancer. Kommerell diverticulitis has not been reported. Diverticulitis, or inflammation/infection of the diverticulum, generally occurs in the colon. It is caused by obstruction, leading to venous congestion, inflammation, and infection. This pathophysiology is unlikely in a vascular structure with active flow such as the Kommerell diverticulum. Although dissection can occur with Kommerell diverticulum, leading to limb ischemia in flow-limiting cases, it would affect the right arm, not the left. Surgical repair of an aberrant right subclavian artery should achieve two main goals: (1) exclusion or repair of any associated Kommerell diverticulum, which may pose a risk for aneurysmal degeneration or rupture, and (2) preservation or restoration of adequate perfusion to the right upper extremity, typically by revascularizing the right subclavian artery.[1,5] Traditionally, this had been done via an open approach, which requires thoracotomy or sternotomy. The diverticulum is then repaired with graft replacement of descending aorta, resection of aneurysm, or aneurysmorrhaphy. The right arm is then revascularized with either carotid to right subclavian bypass or transposition or re-anastomosis of right subclavian artery onto the aortic arch.[1] With the advancement in endovascular techniques in the last two decades, a hybrid approach is becoming more common. It utilizes thoracic endovascular aortic repair (TEVAR) to exclude the Kommerell diverticulum, along with embolization or extra-anatomic bypass or transposition of the right subclavian artery, as mentioned above. This approach spares the patient from the more invasive thoracotomy or sternotomy, as the open portion can be performed via neck incisions only. One potential complicating factor to endovascular repair is the small distance between the origins of the aberrant right subclavian artery and the left subclavian artery (Figure 2), preventing a good proximal seal zone of the stent graft without covering the left subclavian artery. In these cases, such as in this patient, a more advanced aortic stent graft can be used, such as a branched aortic endoprosthesis. This would allow the stent graft to extend into the left subclavian artery to maintain perfusion, achieve adequate seal, and exclude the Kommerell diverticulum (Figure 3). Alternatively, additional extra-anatomic bypass or transposition of the left subclavian artery can be performed. Figure 2. Measurements of distance between aberrant right subclavian artery and left subclavian artery. Figure 3. Kommerell diverticulum before and after repair by stent (a before repair; b and c after repair). The other answers do not completely address the underlying problem, which include both the extrinsic compression of the esophagus by the retroesophageal aberrant right subclavian artery and the Kommerell diverticulum. An esophageal stent would exert additional force on the esophagus that may exacerbate the patient's symptoms, and it does not address the diverticulum. It will also put the patient at risk of stent erosion or migration. Percutaneous gastrostomy tube insertion would help with supplemental nutrition if the patient had severe dysphagia. However, this patient does not have severe dysphagia, and it would not relieve her symptoms or address their underlying cause. Right carotid to subclavian bypass without aortic repair will not exclude the diverticulum, which will continue to be pressurized by the aorta. This patient underwent TEVAR with branched aortic endoprosthesis into the left subclavian artery, followed by right subclavian to right common carotid artery transposition. She had an uneventful postoperative recovery and was discharged after 3 days. At 1-month follow up, her symptoms had resolved, and CT angiography showed excluded and regressed Kommerell diverticulum with patent subclavian arteries bilaterally. Given the rarity of the condition, no guidelines have been developed for follow-up surveillance after repair of aberrant right subclavian artery and Kommerell diverticulum utilizing a hybrid open and endovascular repair. However, because TEVAR was performed, the patient is at risk for the same postoperative complications as when it is performed for other aortic pathologies, so similar approaches can be taken in terms of postoperative surveillance. Current Society for Vascular Surgery guidelines recommend contrast-enhanced CT angiography at 1 month and 12 months after TEVAR for repair of descending thoracic aortic aneurysms, and then yearly for life, with consideration of more frequent imaging if an endoleak or other abnormality of concern is detected at 1-month follow-up.[6]
Washington Post
7 days ago
- Health
- Washington Post
Would you be able to recognize signs of a stroke?
You're reading The Checkup With Dr. Wen, a newsletter on how to navigate medical and public health challenges. Click here to get the full newsletter in your inbox, including answers to reader questions and a summary of new scientific research. Recently, I saw a patient who was recovering from a stroke. She told me she was having breakfast when she realized something was wrong. She kept dropping her spoon because her fingers could no longer grasp it. She took a drink of her coffee and felt liquid dribbling down her chin. When she looked in the mirror, one side of her face sagged.
South China Morning Post
20-05-2025
- South China Morning Post
Patient arrested for indecently assaulting nurse in Hong Kong hospital ward
A patient has been arrested for allegedly indecently assaulting a female nurse at North District Hospital in Hong Kong. Advertisement The nurse, 23, was suspected to have been indecently assaulted in a medical ward at about 4.10pm on Tuesday, the Hospital Authority said. The 59-year-old male patient was receiving treatment at the Sheung Shui hospital. A report about the incident was made at around 7pm, a police spokesman said Officers conducted an initial investigation, believing the suspect and complainant were not acquainted. The man was detained for investigation. Advertisement The case has been handed over to the Tai Po district investigation team.
