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Anxiety Diagnosis
Anxiety Diagnosis

Health Line

time9 hours ago

  • Health
  • Health Line

Anxiety Diagnosis

Key takeaways Diagnosing anxiety requires a comprehensive approach, including a physical examination and a thorough review of your personal history to rule out other medical conditions that may mimic anxiety symptoms. Various self-assessment questionnaires and clinical assessments, such as the Zung Self-Rating Anxiety Scale and the Hamilton Anxiety Scale, are used to evaluate the level and severity of anxiety. Effective management of anxiety involves a combination of medication, therapy, lifestyle adjustments, and open communication with family and friends. Read on to learn more about the process of diagnosing anxiety. During the physical examination You should be completely honest with your doctor. Many things can contribute to or be affected by anxiety, including: certain illnesses medications alcohol consumption coffee consumption hormones Other medical conditions can cause symptoms that resemble anxiety. Many anxiety symptoms are physical, including: racing heart shortness of breath shaking sweating chills hot flashes chest pain twitching dry mouth nausea vomiting diarrhea frequent urination Your doctor may perform a physical exam and order a variety of tests to rule out medical conditions that mimic anxiety symptoms. Medical conditions with similar symptoms include: heart attack angina mitral valve prolapse tachycardia asthma hyperthyroidism adrenal gland tumors menopause side effects of certain drugs, such as drugs for high blood pressure, diabetes, and thyroid disorders withdrawal from certain drugs, such as those used to treat anxiety and sleep disorders substance abuse or withdrawal Diagnostic tests It's suggested that you complete a self-assessment questionnaire before other testing. This can help you decide whether you may have an anxiety disorder or if you may be reacting to a certain situation or event. If your self-assessments lead you to believe that you may have an anxiety disorder, your doctor may then ask you to take a clinical assessment or conduct a structured interview with you. Your doctor may use one or more of the following tests to assess your level of anxiety. Zung Self-Rating Anxiety Scale The Zung test is a 20-item questionnaire. It asks you to rate your anxiety from 'a little of the time' to 'most of the time' on subjects such as: nervousness anxiety shaking rapid heartbeat fainting frequent urination nightmares Once you complete this test, a trained professional assesses your responses. Hamilton Anxiety Scale (HAM-A) Developed in 1959, the Hamilton test was one of the first rating scales for anxiety. It's still widely used in clinical and research settings. It involves 14 questions that rate moods, fears, and tension, as well as physical, mental, and behavioral traits. A professional must administer the Hamilton test. Beck Anxiety Inventory (BAI) The BAI helps measure the severity of your anxiety. You can take the test by yourself. It may also be given orally by a professional or paraprofessional. There are 21 multiple-choice questions that ask you to rate your experience of symptoms during the past week. These symptoms include tingling, numbness, and fear. Answer options include 'not at all,' 'mildly,' 'moderately,' or 'severely.' Social Phobia Inventory (SPIN) This 17-question self-assessment measures your level of social phobia. You rate your anxiety in relation to various social situations on a scale from zero to four. Zero indicates no anxiety. Four indicates extreme anxiety. Penn State Worry Questionnaire This test is the most widely used measure of worry. It distinguishes between social anxiety disorder and generalized anxiety disorder. The test uses 16 questions to measure your worry's generality, excessiveness, and uncontrollability. Generalized Anxiety Disorder Scale This seven-question test is a screening tool for generalized anxiety disorder. You're asked how often in the past two weeks you've been bothered by feelings of irritability, nervousness, or fear. Options include 'not at all,' 'several days,' 'more than half the days,' or 'nearly every day.' Yale-Brown Obsessive-Compulsive Scale (YBOCS) The YBOCS is used to measure levels of OCD. It's conducted as a one-on-one interview between you and a mental health professional. You choose three items from a symptom checklist that are the most disturbing and then rate how severe they are. Then, you're asked whether you've had certain other obsessions or compulsions in the past. Based on your answers, the mental health professional grades your OCD as subclinical, mild, moderate, severe, or extreme. Mental health disorders that feature anxiety Anxiety is a symptom in several disorders. Some of these include: Disorder Symptoms Panic disorder High amounts of anxiety as well as physical stress for a short amount of time; physical stress can come in the form of dizziness, a high heart rate, sweating, numbness, and other similar symptoms Obsessive-compulsive disorder (OCD) Anxiety expressed as obsessive thoughts or as compulsive behavior that's acted upon repeatedly to relieve stress Phobias Anxiety triggered because of a specific thing or situation that isn't necessarily harmful or dangerous, including animals, heights, or riding in vehicles Social phobias Anxiety that's experienced in interpersonal situations, such as during conversations, in large social groups, or when speaking in front of a crowd The broadest anxiety disorder, generalized anxiety disorder (GAD), is different from these other disorders because it doesn't necessarily relate to a specific cause or behavior. With GAD, you may worry about many different things at once or over time, and the worries are often constant. Diagnostic criteria An anxiety diagnosis depends a lot on your description of the symptoms you're experiencing. Mental health professionals use the 'Diagnostic and Statistical Manual of Mental Disorders' (often called the DSM) to diagnose anxiety and other mental disorders based on symptoms. The criteria differ for each anxiety disorder. The DSM lists the following criteria for generalized anxiety disorder (GAD): excessive anxiety and worry most days about many things for at least six months difficulty controlling your worry appearance of three of the following six symptoms: restlessness, fatigue, irritability, muscle tension, sleep disturbance, and difficulty concentrating symptoms significantly interfering with your life symptoms not being caused by direct psychological effects of medications or medical conditions symptoms aren't due to another mental disorder (e.g. anxiety about oncoming panic attacks with panic disorder, anxiety due to a social disorder, etc.) Anxiety diagnosis in children Childhood and the teenage years are full of new, frightening experiences and events. Some children learn to confront and accept these fears. However, an anxiety disorder can make it difficult or impossible for a child to cope. The same diagnostic criteria and assessments that are used for adults apply to children, too. In the Anxiety and Related Disorders Interview Schedule for DSM-5 (ADIS-5), your doctor interviews both you and your child about their symptoms. Symptoms in children are similar to those in adults. If you notice anxiety symptoms or any anxious or worrying behaviors that last for more than two weeks, take your child to the doctor. There, they can be checked for an anxiety disorder. Some research suggests that anxiety can have a genetic component. If anyone in your family has ever been diagnosed with anxiety or a depressive disorder, get your child evaluated as soon as you notice symptoms. A proper diagnosis can lead to interventions to help them manage anxiety at a young age. What to do if you're diagnosed with anxiety Focus on managing your anxiety rather than on ending or curing it. Learning how best to control your anxiety can help you live a more fulfilled life. You can work on stopping your anxiety symptoms from getting in the way of reaching your goals or aspirations. To help manage your anxiety, you have several options. Medication If you or your child is diagnosed with anxiety, your doctor will likely refer you to a psychiatrist who can decide what anxiety medications will work best. Sticking to the recommended treatment plan is crucial for the medications to work effectively. Try not to delay your treatment. The earlier you begin, the more effective it will be. Therapy You might also consider seeing a therapist or joining a support group for people with anxiety so that you can talk openly about your anxiety. This can help you control your worries and get to the bottom of what triggers your anxiety. Lifestyle choices Find active ways to relieve your stress. This can lessen the impact that anxiety may have on you. Some things you can do include: Get regular exercise. Find hobbies that engage or occupy your mind. Participate in activities that you enjoy. Keep a daily journal of thoughts and activities. Create short-term or long-term schedules. Socialize with friends. Also, avoid alcohol, nicotine, and other similar drugs. The effects of these substances can make your anxiety worse. Communication Be open with your family and close friends about your diagnosis, if possible. It's not easy to talk about any mental disorder. However, the more the people around you understand your anxiety, the easier it becomes to communicate your thoughts and needs to them. Anxiety relief tips Stick to the treatment plan recommended by your psychiatrist. Consider seeing a therapist or joining a support group for people with anxiety. Find active ways to relieve your stress, such as getting regular exercise or keeping a daily journal. Be open with your family and close friends about your diagnosis, if possible. Avoid alcohol, nicotine, and other similar drugs. Focus on managing your anxiety rather than on ending or curing it.

Uncontrolled Movements, Anger, and Insomnia
Uncontrolled Movements, Anger, and Insomnia

Medscape

time13 hours ago

  • Health
  • Medscape

Uncontrolled Movements, Anger, and Insomnia

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 35-year-old man presents to the neurology clinic due to abnormal movements over the past 6 years. The involuntary movements began in the right upper limb, followed sequentially by the left upper limb, left lower limb, and finally the head and neck. The movements occur during wakefulness and are absent in sleep. They are described as jerky and nonpurposeful. His gait has assumed a dancelike character. He also has had behavioral changes that include frequent outbursts of anger, aggressive behavior, depressive mood, and insomnia. His abnormal movements are aggravated during outbursts of anger and disturbances in mood. He has no weakness in any limbs but is unable to perform regular household activities. Family members have also noted memory impairment. He has been unable to continue his work as a machine operator for the past 3 months. He has no history of psychoactive drug intake, including phenytoin, phenothiazines, haloperidol, L-dopa, lithium, isoniazid, amphetamines, tricyclic antidepressants, or any other relevant drugs. He reports no history of chest pain, breathlessness, or joint pain. His family history includes a paternal grandfather and father who had similar forms of abnormal movements and died at the age of 60 years and 55 years, respectively. The patient has five siblings (two brothers, three sisters). His elder brother died by suicide at age 25 years, and his elder sister died at age 33 years. Both had abnormal movements and abnormal behaviors. One of his younger sisters (age 22 years) also has similar abnormal movements and depressed attitude. His younger brother (age 17 years) and other younger sister (age 14 years) are healthy and symptom-free. The patient's children, an 8-year-old son and a 10-year-old daughter, are symptom-free. His past medical history is positive for hypertension, which is well controlled with lisinopril (20 mg daily). He has no surgical history. He does not smoke, drink, or use recreational drugs. Physical Examination and Workup A general examination reveals a pleasant man who is well built and in no acute distress. His blood pressure is 140/80 mm Hg, his heart rate is 78 beats/min, his respiratory rate is 12 breaths/min, his SpO 2 level is 98% on room air, and his body mass index (BMI) is 20. He is afebrile. A cardiovascular examination reveals normal peripheral pulses and normal heart findings. A chest examination reveals normal auscultation and expansion. His abdomen is soft. Head, eyes, ears, nose, and throat (HEENT) examination findings are unremarkable. He does not have a skin rash. A visual examination reveals normal acuity, field, and fundi. His affect is flat. A neurologic examination of the higher mental functions reveals that the patient is awake and alert, with normal orientation, attention, concentration, fund of knowledge, and language function. His memory is impaired, with recall one-third at 3 minutes. He has a normal past memory. His speech is normal. A cranial nerve examination reveals normal extraocular movements, increased blink rate, normal facial sensation, a symmetric face with abnormal fidgety movement, normal hearing, and normal palate movement. He has abnormal tongue movement and cannot protrude his tongue more than 20 seconds (darting tongue movement). He has normal shoulder shrug. No Kayser-Fleischer ring is noted during slit-lamp examination. An examination of the motor system reveals decreased muscle tone, normal bulk, and 5/5 strength in both upper and lower extremities. No atrophy or fasciculation is noted. Deep tendon reflexes are normal (2+ with flexor planters). Sensory examination findings are normal. Finger-nose test findings are normal. An examination of the extrapyramidal system reveals reduced tone and involuntary choreoathetoid movements that affect both upper and lower extremities as well as his face. He has a dancing gait. Diagnostic tests reveal normal complete blood cell count (CBC) and comprehensive metabolic panel findings. He has normal serum findings and urine copper levels. His erythrocyte sedimentation rate (ESR) is 22 mm/hr (reference range, 0-22 mm/hr). He has normal ECG findings, a normal thyroid-stimulating hormone (TSH) level, a normal transthoracic echo (with ejection fraction 65%), and normal chest radiography findings. Brain MRI can be used to evaluate for selective atrophy of deep gray structures, to document disease burden, and to provide a baseline for future comparison. Whole-body 18-FDG PET/CT may be used to screen for occult neoplasm and paraneoplastic chorea, but this is exceedingly rare and typically subacute. NMDA receptor antibody panel may be used to investigate for autoimmune encephalitic chorea, but the features of this (ie, seizures, psychosis, and autonomic instability) are absent in this case. RPR and FTA-ABS may be used to evaluate for neurosyphilitic chorea, but this is also very uncommon and unnecessary without risk factors or acute symptoms. In this patient, brain MRI reveals evidence of bilateral caudate atrophy, with increased intercaudate distance (Figure). Figure. Cerebrospinal fluid (CSF) examination findings are normal. Discussion This 35-year-old man has Huntington disease. He has insidious-onset, slowly progressive movement disorder, and movements are absent during sleep. His movements are described as choreoathetoid. He has family history that suggests autosomal dominant transmission. Apart from the movement disorder, he also has neuropsychiatric manifestations, with death at an early age in the family. A CT scan of the head revealed evidence of caudate nucleus atrophy. Brain MRI revealed evidence of caudate atrophy (Figure). Figure. In evaluating the differential diagnoses, the patient has no history of antipsychotic medication use to suggest tardive dyskinesia. He has no clinical or diagnostic evidence of infection or heart involvement, which makes Sydenham chorea unlikely. No acanthocytes were observed, helping to exclude neuroacanthocytosis. The strong family history of progressive abnormal movements and neuropsychiatric symptoms across generations supports a genetic etiology, specifically autosomal-dominant Huntington disease. Huntington disease is a rare neurodegenerative disorder of the central nervous system (CNS) characterized by choreiform movements, behavioral and psychiatric disturbances, and dementia.[1] Huntington disease is caused by an autosomal-dominantly inherited expansion of CAG trinucleotide repeats in the huntingtin ( HTT ) gene on chromosome 4; this leads to production of a mutant huntingtin (mHTT) protein, with an abnormally long polyglutamine repeat.[2] Individuals with more than 39 CAG repeats develop the disease, whereas reduced penetrance is seen in those with 36-39 CAG repeats. The disease can be anticipated when the gene is passed down the paternal line, as in this case; a father with a CAG repeat length in the intermediate range may have a child with an expanded pathogenic repeat length. This is because sperm from males shows greater repeat variability and larger repeat sizes than somatic tissues. Mutant huntingtin protein leads to death and neuronal dysfunction through various mechanisms. Postmortem studies reveal diffuse atrophy of the caudate and putamen. The progressive worsening of Huntington disease leads to a bedridden state with cognitive deterioration, and death typically occurs about 20 years after the onset of symptoms.[3] Prevalence in the white population is estimated at 1 in 10,000 to 1 in 20,000. The mean age at symptom onset is 30-50 years. In some cases, symptoms begin before age 20 years, with behavior disturbances and learning difficulties at school; this is termed juvenile Huntington disease (Westphal disease).[4] The first description, by Waters, dates to 1842. However, after a description in 1872 by George Huntington, it became known as Huntington chorea. In 1983, a linkage on chromosome 4 was established, and in 1993 the gene for Huntington disease was found.[1] Diagnosis of Huntington disease is confirmed by demonstration of autosomal dominant transmission or gene testing in the presence of clinical features.[5] The clinical features of Huntington disease consist of motor, cognitive, and neuropsychiatric manifestations. Huntington disease has a biphasic course of hyperkinetic phase with chorea in the early stages of disease that then plateaus into a hypokinetic phase, consisting of bradykinesia dystonia, balance issues, and gait disturbance. The younger-onset variant is associated with predominant bradykinesia.[6] Cognitive disturbance can be seen many years before other symptom onset and is characterized by impaired emotion recognition, processing speed, and executive function abnormality. Neuropsychiatric symptoms widely vary, including apathy, anxiety, irritability, depression, obsessive-compulsive behavior, and psychosis. A lack of awareness of early and progressing behavioral, cognitive, and motor symptoms is a hallmark of Huntington disease. This unawareness is caused by the disease itself (specifically, impaired insight or anosognosia) and is not the result of intentional denial, avoidance, or suppression of symptoms.[7] Therefore, a comprehensive history, including information from a knowledgeable family member/caregiver, is advisable.[7] Numerous conditions can mimic Huntington disease, including a spinal cerebellar ataxia 17, spinocerebellar ataxia 1-3, and Friedreich ataxia, which involve neuropathy. If seizures are also present, dentatorubropallidoluysian atrophy should be considered. Acanthocytes are seen in patients with neuroacanthocytosis.[8-10] Isolated chorea can be seen in acquired conditions, including chorea gravidarum, systemic lupus erythematosus, antiphospholipid syndrome, thyrotoxicosis, postinfectious syndromes, polycythemia vera, and some drug use. Genetic testing for the mHTT mutation can be either diagnostic or predictive.[6] A diagnostic test may be performed when a patient presents with typical motor features of Huntington disease. Prior to testing, the patient should be informed about Huntington disease and its hereditary nature, as a positive test result has implications for the patient and family. Predictive testing is performed in asymptomatic patients, mostly for reproductive reasons. Treatment of Huntington Disease The optimal management of Huntington disease involves a multidisciplinary approach that includes neurology, nurses, physical therapy, speech-language pathology, and dietitians and other healthcare professionals. The goal is to optimize the quality of life based on the changing need of the patient. These consist of combined pharmacologic and lifestyle changes, including behavioral therapy. Symptoms may be worsened by stress, fatigue, and intercurrent disorders (eg, anxiety, digestive disorders, infectious or painful conditions), so these aspects must be assessed and treated alongside the primary symptoms of Huntington disease.[3] In clinical practice, information about symptoms should be obtained from both the patient and caregivers, since patients may have impaired awareness of their condition.[11] Identifying coexisting psychiatric symptoms, comorbid medical conditions, and environmental factors is crucial.[11] Educating caregivers about the nature and presentation of symptoms and methods to modify triggers is also vital.[11] Medication choices should be guided by coexisting symptoms and disease stage, and regular reassessment of drug need and potential for dose reduction is important because of adverse effects that can mimic disease progression.[11] Nonpharmacologic interventions, including behavioral therapies and environmental modifications, should be prioritized for neuropsychiatric symptoms in Huntington disease. Pharmacologic agents may be considered if these measures are insufficient, and consultation with a psychiatrist knowledgeable in Huntington disease is recommended for individuals whose symptoms are resistant to standard pharmacologic therapy.[11] Tetrabenazine and its modified version, deutetrabenazine, are commonly used to treat choreiform movements. Side effects of tetrabenazine can include depression, anxiety, sedation, sleep problems, restlessness, and parkinsonism.[7] Citalopram is a selective serotonin reuptake inhibitor used to manage depression. Modafinil and atomoxetine are used to manage apathy. Tiapride, although unavailable in the United States, is considered a first-line treatment option for chorea outside the United States.[7] Other antipsychotics such as olanzapine, risperidone, and quetiapine are also used to manage chorea. Risperidone may also help with psychomotor restlessness, and olanzapine and quetiapine can have additional benefits like weight gain (which can be desirable in Huntington disease) and mood stabilization. Haloperidol has also shown effectiveness.[7] Medications used to suppress chorea (eg, tetrabenazine and deutetrabenazine and certain antipsychotics) should be used sparingly and mainly for subjectively disabling hyperkinesias, starting at low doses and titrating gradually. They make take 4-6 weeks to show results.[7] The choice of medication depends on the individual patient's symptoms, tolerability, and co-existing conditions.[7] Evidence regarding the treatment of psychiatric symptoms in Huntington disease is limited, with recommendations often based on expert opinion owing to a lack of robust controlled studies.[7,11] Nonpharmacologic interventions such as cognitive-behavioral therapy and psychodynamic therapy are recommended, especially for depression, anxiety, obsessive-compulsive behaviors, and irritability. Behavioral strategies (eg, structured routines and distraction) are important for managing irritability and agitation.[3,11] Depression: Selective serotonin reuptake inhibitors (SSRIs) such as citalopram, fluoxetine, paroxetine, sertraline, and venlafaxine are recommended as pharmacologic options. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. [3,7,11] Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. [3,7] Mianserin (unavailable in the United States) or mirtazapine are alternatives, particularly in patients with sleep disruption. Electroconvulsive therapy (ECT) may be considered for severe or resistant cases, although it can significantly impair short-term memory. Anxiety: SSRIs or serotonin-noradrenaline reuptake inhibitors (SNRIs) are first-line treatments, especially when anxiety coexists with depression. [3,11] Mirtazapine is an option in patients with sleep disorders. [11] Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. [3,11] Mirtazapine is an option in patients with sleep disorders. Long-term use of benzodiazepines is generally discouraged for ambulatory individuals because of the risk of falls and dependence but can be used short-term or as needed. Obsessive-compulsive behaviors/perseverations: For true obsessive-compulsive phenomena, SSRIs are considered first-line treatment. [3] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. [3] Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. [11] Olanzapine and risperidone may also be valuable for ideational perseverations, particularly if associated with irritability. Clomipramine is an option, especially if needed for coexisting obsessive perseverative behaviors. Irritability and aggression: SSRIs are a first-line treatment. [3] For aggressive behavior, neuroleptics are recommended. [3,7] Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. [3,7] For aggressive behavior, neuroleptics are recommended. Mood stabilizers (eg, valproate, lamotrigine, lithium, carbamazepine) can be added if irritability is resistant to other treatments or for mood lability. Risperidone and olanzapine may help reduce irritability. Psychosis (hallucinations/delusions): Second-generation neuroleptics (antipsychotics) are the first-line pharmacologic treatment. [3,7,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. [7] Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. [3,7,11] Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. [3,11] Options include olanzapine, risperidone, quetiapine, aripiprazole, and haloperidol. Clozapine may be considered for severe or resistant cases, particularly in akinetic forms of Huntington disease but requires regular monitoring. Underlying causes, such as the use of psychotropic agents or somatic triggers, should be investigated and addressed. Apathy: Personalized cognitive stimulation and structured routines and activities are recommended.[3,7,11] If depression is suspected as a contributor, an SSRI should be tried.[3,11] In patients without depression, activating antidepressants or stimulant drugs (eg, methylphenidate, atomoxetine, modafinil) may be considered.[11] Sedative medications may increase apathy, so their dosage should be monitored or reduced.[3,11] Currently, no pharmacological treatment is specifically recommended for cognitive symptoms in Huntington disease.[3,7] Rehabilitation strategies, including speech therapy, occupational therapy, cognitive and psychomotor therapy, may help transiently improve or stabilize cognitive functions.[3,7] Coping strategies can be useful as an alternative to medication. Certain medications, such as sedative drugs, neuroleptics, and tetrabenazine, can negatively affect memory, executive functions, and attention.[3] Apart from symptomatic treatment, pharmacologic agents have failed to show benefit in clinical trials as disease-modifying agents. The most promising approaches in regard to disease modification are emerging therapies aimed at lowering levels of mHTT by targeting either the DNA or RNA of the mHTT gene.[12] RNA-targeting using antisense oligonucleotides (ASOs) have shown disappointing results in clinical trials. This has shifted significant research focus and toward orally available small molecules that modify HTT mRNA splicing, thereby reducing mHTT protein production. DNA-targeting approaches using gene editing tools like CRISPR/Cas9, while demonstrating success in preclinical models, remain in the early stages of development.[13,14] The patient in this case was diagnosed with Huntington disease with CAG repeat 78. He was started on tetrabenazine for abnormal movements and citalopram for depression. He opted to apply for federal disability. His children are asymptomatic, and the family decided not to investigate until symptoms develop or they are age 18 years.

Aussie woman's horror 25 hours in an emergency department waiting room exposes the huge problem with our healthcare system
Aussie woman's horror 25 hours in an emergency department waiting room exposes the huge problem with our healthcare system

Daily Mail​

timea day ago

  • Health
  • Daily Mail​

Aussie woman's horror 25 hours in an emergency department waiting room exposes the huge problem with our healthcare system

A young woman has documented the 25 hours she spent by her ailing mother's side as she desperately waited for a bed in a Sydney emergency department. Ella Jae, 22, shared a video of her time in the waiting room of Westmead Hospital, in Sydney's west, to social media last week. She said her mother, who was suffering health problems after having an abscess removed, and elderly patients were forced to endure an entire day and 'freezing' night in the hospital before being given a bed. She started filming about four hours into her wait, at 10pm. 'The amount of people in this waiting room is absolutely crazy,' she said while sitting outside the hospital, rugged up in a hoodie and tracksuit pants. 'I feel terrible for all of them because there are people that have been waiting for 12 hours.' It would be another 21 hours before her mother was given somewhere to lie down, after an entire night and day of agony. 'I've never had an experience like this before,' Ms Jae said at the 22-hour mark. 'Pretty devastated at the Australian government right now.' Ms Jae shared various updates throughout the night, such as at the 1.30am mark where she had to renew her parking, and said her mum was given some pain relief. She provided another update at 2.30am and one at 4.30am, wrapped in blankets, where she said her mother was finally seen by a doctor but had to return to the waiting room. More hourly updates were given until her mother was finally taken in, more than a day later. The video casts doubt over efforts to tackle the state's overstretched public hospital system, including a recent $900million redevelopment of Westmead. Half the emergency patients at Westmead waited at least 6.5 hours in July to September last year, the longest in the state, according to hospital data. The problem is even more pronounced in mental health emergency care, with one schizoaffective patient reportedly waiting 93 hours for a bed at the hospital in April. He was forced to wait alongside two other men - one with paranoid ideation and another with schizophrenia - who reportedly waited 88 hours and 86 hours for beds. Their stories were the subject of a June expose by the ABC's Four Corners program. It comes after distressing images emerged of elderly patients lying on the floor of Blacktown Hospital, some waiting hours while in pain. Among them was Raymond, a 70-year-old man, who presented to the western Sydney hospital's waiting room on Saturday with severe diarrhoea and life-threatening haemoglobin levels. Despite his condition, he spent more than 24 hours waiting for a bed - much of it trying to sleep on the cold, hard vinyl floor of the waiting room in excruciating pain. His daughter Hayley took a photo of him during the agonising wait and shared it with 2GB Breakfast host Ben Fordham. She also shared a photo of another elderly man, 80, sleeping on the floor, wrapped in a blanket. The man had already been waiting for a bed for at least 12 hours. 'No one wants to see the elderly suffer in pain like this,' she said. The images indicate little has been done in the ten months since Premier Chris Minns singled out Blacktown as he vowed to improve the state's public health system. 'We'll have to look at Blacktown in particular - there's major stress on our public hospitals,' Minns said last September. 'We want to do better when it comes to health outcomes.'

I'm an eye doctor and this is the dangerous condition on the rise that everyone is missing... you must take this simple precaution to save your vision as you age
I'm an eye doctor and this is the dangerous condition on the rise that everyone is missing... you must take this simple precaution to save your vision as you age

Daily Mail​

time2 days ago

  • Health
  • Daily Mail​

I'm an eye doctor and this is the dangerous condition on the rise that everyone is missing... you must take this simple precaution to save your vision as you age

Examining his patient's red, painfully inflamed eye, Australian ophthalmologist Emil Kurniawan was in no doubt that she had a pterygium, a benign but potentially vision-altering growth on the surface of the eye. Linked to prolonged UV exposure, it is commonly found in people living in sunny regions – including many parts of Australia.

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