Basic Asthma Management (Coreem)

Definition: An episode of wheezing, chest tightness or coughing resulting from variable airflow obstruction that is reversible. Underlying exacerbations is a chronic inflammatory disorder of the airways.

Epidemiology:

• 1 million Americans suffer from asthma
• 75 million ED visits/year
• 456,000 hospitalizations in the US (Akinbami 2011)

Pathophysiology:

• Stimuli (allergen and non-allergen) induce bronchoconstriction
• Bronchoconstricting stimuli result in edema, inflammation, airway smooth muscle hypertrophy and mucous production.
• Long-term permanent structural airway remodeling can develop
• Airway inflammation limiting airflow is the common final pathway

Symptoms:

• Wheezing
• Cough
• Dyspnea
• Chest tightness
• Shortness of Breath

Physical Exam

• Wheezing
• Tachypnea
• Tachycardia
• Retractions
• Use of accessory respiratory muscles
• Speaking in short sentences

Immediate Management:

Basics: ABCs with a focus on breathing. Supplementary O2 typically not needed in mild to moderate exacerbations.

Inhaled Beta2 Agonist (i.e. albuterol)

• Mechanism: Stimulate beta2 receptors in lungs leading to bronchodilation
• Nebulized albuterol solution
  • Dose:5 mg every 10-20 min
  • Can be paired with an inhaled anticholinergic
• Albuterol metered-dose inhaler (MDI)
  • Equally effective to nebulized solution in mild exacerbations (Newman 2002, Cates 2013)
  • Dose: 6-12 puffs every 10-20 min
• Side effects: tachycardia (beta1 stimulation), tremors, lactic acidosis (Lewis 2014)

Inhaled Anticholinergic (i.e. Ipratropium)

• Mechanism: Override smooth muscle constriction and secretory consequences of parasympathetic nervous system. Block reflex bronchoconstriction.
• Dose: 0.5 mg every 10-20 min (up to 3 doses)
• Impact: In combination with beta2 agonist, may avoid hospitalization in up to 1 in 11 treated patients (Plotnick 1998).

Systemic Corticosteroids

• Mechanism: Inhibit recruitment of inflammatory cells and mediators.
• Route: Evidence suggests that oral and intravenous corticosteroids are equally efficacious in patients with mild to moderate asthma exacerbations
• Dose
  • Prednisone: 1 mg/kg (typically up to 60 mg) PO
  • Methylprednisolone sodium: 125 – 250 mg IV or IM
  • Dexamethasone: 10-20 mg PO
• Impact: Numerous studies have shown reductions in admission rates as a result of systemic corticosteroid use in the ED (Rowe 1992). The majority of patients presenting to an ED for asthma exacerbation should receive systemic steroids.

Magnesium 

• Mechanism: Bronchial smooth muscle relaxation
• Dose: 1-2 g over 30-60 min
• Impact: Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014)
• Reserved for moderate to severe exacerbations

Special Populations: Pregnancy

• Acute asthma exacerbations should be treated the same in pregnant patients as in nonpregnant patients.
• Fetal monitoring should be considered for patients with moderate to severe exacerbations in the 3rd

Diagnostics: Asthma is a clinical diagnosis and patients with mild to moderate exacerbations rarely need any testing in the ED. Diagnostic tests may be useful in patients with asthma that is refractory to standard management as detailed above or if an alternate cause of symptoms is suspected.

Pulmonary Function Tests (PFTs)

• Measure forced expiratory volume in 1 second (FEV1) or peak expiratory flow rate (PEFR)
• Most helpful when patient knows their baseline performance

Chest Radiography

• The majority of patients with asthma exacerbations that are typical for them do not need a chest X-ray performed.
• Consider X-ray in patients with more severe symptoms or those that do not resolve with standard treatment.

Lab Studies

• Rarely useful in mild to moderate (or even in severe) asthma exacerbations.
• Leukocytosis common as a result both of stress as well as steroid use
• Arterial Blood Gas
  • Do not correlate with clinical outcomes
  • Critical ABG data points (O2, CO2) can be obtained by other means (Pulse oximetry for O2, VBG for CO2)

Disposition

• Relapse after ED visits is common (up to 11% at 3 days) (Rosen’s 2014)
• Admission
  • Incomplete response based on overall clinical picture or PFTs (< 70% improvement)
  • Significant comorbidities
• Discharge
  • Airway inflammation continues after discharge and can take days to improve
  • Medications
    • Beta agonist inhaler (and demonstration of proper use). Consider giving all patients a spacer device as this improves drug delivery and thus efficacy.
    • Steroids
      • Short burst steroid treatment with prednisone for 5 days (no taper needed)
      • Dexamethasone – 2 doses on days 1 and 2 shown to be non-inferior to 5 days of prednisone in one small study (Kravitz 2011)
    • Follow-up
      • Patients should contact their physician in 3-5 days and have follow-up arranged in 1-2 weeks
      • Consider referral to an asthma specialist in patients with frequent exacerbations, frequent ED visits or frequent rescue inhaler use.

Take Home Points

• First line treatment for asthma exacerbations is inhaled beta agonists, inhaled anticholinergics and systemic corticosteroids.
• The majority of patients presenting to the ED with asthma exacerbations should be started on short-burst corticosteroids to control inflammation and prevent admission and relapse.
• Diagnostic testing is not required for the majority of patients with asthma exacerbations.

References:

1. Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58
2. Akinbami LJ et al. Asthma prevalence, health care use, and mortality: United States, 2005-2009. Natl Health Stat Report 2011; 32:1-14. Link
3. Newman KB et al. A comparison of albuterol administered by metered-dose inhaler and spacer with albuterol by nebulizer in adults presenting to an urban emergency department with acute asthma. Chest 2002; 121: 1036-41. PMID: 11948030
4. Cates CJ et al. Holding chambers (spacers) versus nebulisers for beta-agnonist treatment of acute asthma (Review). Cochrane Database Syst Rev 2013. PMID: 24037768
5. Lewis LM et al. Albuterol administration is commonly associated with increases in serum lactate in patients with asthma treated for acute exacerbations of asthma. Chest 2014; 145(1): 53-9. PMID: 23949578
6. Plotnick LH, Ducharme FM. Should inhaled anticholinergic be added to B2 agonists for treating acute childhood and adolescent asthma? A systematic review. BMJ 1998; 317: 971-7. PMID: 9765164
7. Rowe BH et al. Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis. Am J Emerg Med 1992; 10: 301-10 PMID: 1535500
8. Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007
9. Kravitz J et al. Two days of dexamethasone versus 5 days of prednisone in the treatment of acute asthma: a randomized controlled trial. Ann Emerg Med 2011; 58: 200-4. PMID: 21334098

This post was initially posted at coreem. Shared with permission. 

Life-Threatening Asthma (Coreem)

Background: Acute severe asthma or status asthmaticus refers to an episode of bronchoconstriction that is unresponsive to standard management. Patients with acute severe asthma will present with significant respiratory distress and it is critical to rapidly treat them to avoid significant morbidity and mortality. Patients will present with tachypnea, retractions, diaphoresis, ability to only speak 1-2 words at a time, abdominal breathing, cold extremeties. and wheezing (although the most severe may have a “quiet chest” indicating the absence of any significant air entry).

Immediate Management:

There are three main goals of immediate management of the severe asthma exacerbation:

1. Stave off intubation while your medications have time to act. Intubation is associated with increased morbidity and mortality.
2. Maximize pre-intubation parameters in case the patient doesn’t turn around and intubation is required.
3. Reverse bronchoconstriction to decrease work of breathing and prevent respiratory failure from exhaustion of respiratory muscles.

Basics: ABCs, IV, supplemental O2. Patient should be provided with all of the therapies used in mild to moderate asthma exacerbations but will require more aggressive management

Oxygenation + Respiratory Support

• Hypoxia only occurs late in a patient with a severe asthma exacerbation. Do not wait for hypoxia before supplying supplemental O2.
• Standard Nasal Cannula – Turn up to 15-20 L/min
• High-Flow Nasal Cannula (HFNC)
  • Allows for increased flow (40-60L/min of humidified O2 
  • May be difficult to administer nebulizer treatments via facemask does not fit over HFNC
• Non-Rebreather with Beta-Agnoist Reservoir
• Non-invasive Positive Pressure Ventilation (NIPPV)
  • Decreases work of breathing and improves gas exchange
  • The evidence demonstrating a benefit to NIPPV is limited but available studies do not show substantial adverse events (Pollack 1995, Soroksky 2003, Lim 2012). These studies did not include the sickest subset of patients with asthma
  • Bilevel Positive Airway Pressure (BPAP) preferred over Continuous Positive Airway Pressure (CPAP)
    • Difference in inspiratory (IPAP) and expiratory (EPAP) pressure aids in increasing tidal volume delivered
    • Start at IPAP 10 mm Hg, EPAP 5 mm Hg (or less) and titrate IPAP up (Typically no need to increase EPAP).

Intravenous Fluids

• Patients with severe asthma exacerbations have enormous insensible losses from increased respirations and work of breathing.
• Lung hyperinflation decreases pulmonary venous return, which can lead to hypotension. This is exacerbated by mechanical ventilation as the patient converts from negative pressure ventilation to positive pressure ventilation thus increasing intrathoracic pressure which can further decrease venous return.
• Aggressive IV fluids (30 cc/kg) should be given early to replete intravascular volume.

Epinephrine

• Epinephrine is a non-selective beta agonist that causes bronchodilation, vasoconstriction, increased cardiac contractility and increased heart rate
• Patients with severe asthma may have minimal benefit from inhaled beta agonists (i.e. albuterol) due to severe bronchoconstriction limiting delivery of medication to distal bronchioles.
• Intramuscular (IM) / Subcutaneous(SQ) Epinephrine
  • Dose: 300-500 mcg
  • Limited evidence demonstrates minimal significant side effects at this dose (Cydulka 1988)
• Intravenous (or Intraosseous) Epinephrine
  • More rapidly reaches target tissue than IM/SQ especially if patient hypotensive
  • Has effect of bronchodilation as well as vasoconstriction, which can reduce airway edema (Grandordy 1995)
  • Dose: 1 – 5 mcg/min and titrate to effect
  • Multiple retrospective studies demonstrate minimal adverse events with IV epinephrine (Smith 2003, Putland 2006)
• Contraindications: Epinephrine can theoretically cause uterine vasoconstriction and should be used with caution in pregnant patients.
• Terbutaline
  • Selective, parenteral beta 2 agonist that causes bronchodilation without effecting heart rate or cardiac output
  • Subcutaneous (SC) Terbutaline: 0.5 mg SC every 4 hours

Magnesium

• Mechanism: Bronchial smooth muscle relaxation
• Impact:
  • Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014). However, the sickest subset of patients were excluded from this study
  • The 3Mg trial (Goodacre 2013) demonstrated only a weak benefit to IV Magnesium in severe asthma however, this study did not include patients with life-threatening asthma.
  • In the absence of robust evidence, it is reasonable to administer magnesium to severe asthma exacerbations as there are minimal side effects of the drug and a potential for benefit
• Dose: The dose in severe asthma is not established. 2 g IV over 15 minutes is a reasonable first dose and this may be repeated

Heliox

• Mechanism: Improved laminar flow of inhaled has which may allow better airflow through the constricted airways; allows better gas exchange and transport of medications to flow down to distal airways and alveoli
• A mixture of helium and oxygen(multiple possible rations – 60:40, 70:30, 80:20). Only give the minimum FiO2 necessary to achieve goal O2saturation
• Evidence of utility limited but has not been extensively studied in the sickest subset of asthmatic patients and may still be beneficial in this group.
• Heliox may be used both via NIPPV and mechanical ventilator
• Limitation: If patient markedly hypoxic, may not give an adequate amount of FiO2.

Intubation

• Only about 2% of asthma exacerbations require intubation with 10-30% of those admitted to the ICU requiring invasive ventilation (Rosen’s 2014)
• Intubation is an inherently dangerous intervention in asthma because it does not fix the underlying problem (bronchoconstriction) and can cause dynamic hyperinflation (see below under ventilation), and rapid acidosis if respiration is not matched during RSI or post-intubation
• There is no specific vital sign, lab value or other diagnostic test result, which determines the necessity for intubation. The decision to intubate is based on a number of factors including the patients overall appearance, work of breathing, perceived ability to maintain their effort of breathing, mental status etc.
• Prior to intubation, be sure to maximize pre-oxygenation and intravascular volume
• Delayed Sequence Intubation (RSI)
  • Procedural sedation (with dissociative dose ketamine) for the procedure of pre-oxygenation
  • Useful in patients who have significant hypoxia/hypercarbia despite resuscitation and do not tolerate NIPPV to aid in pre-oxygenation
  • See the EMCrit website for full details on the procedure
• Rapid Sequence Intubation (RSI) Medications
  • There is no optimal set of agents for RSI in the severe asthmatic
  • Ketamine
    • Preferred agent because it is relatively hemodynamically stable and it has bronchodilatory properties.
    • Dose: 1-2 mg/kg
  • Paralytic
    • Common options are rocuronium and succinylcholine
    • Rocuronium offers the advantage of longer paralysis which avoids vent asynchrony early in management

Mechanical Ventilation

• Appropriate mechanical ventilation relies on ensuring that the patient has an adequate time to fully expire the delivered breath and avoid hyperinflation
• Permissive Hypercapnea: Decreasing respiratory rate and allowing PaCO2 to rise to supranormal levels.
  • This strategy avoids breath stacking which leads to hyperinflation
  • Hyperinflation leads to increased airway pressures and can lead the development of a tension pneumothorax
  • Hyperinflation can also lead to marked decrease in venous return leading to decreased cardiac output and cardiac arrest
  • Hyperinflation leads to increased pulmonary vascular resistance and right ventricular dysfunction
• Post-intubation meds (A full discussion of post-intubation care will appear in a future post)
  • Analgesia
    • Fentanyl (1-2ug/kg/hr) preferred over morphine or hydromorphone as it has minimal histamine effects
  • Sedation Options: Ketamine, propofol
  • Consider short-term paralysis if difficulty ventilating the patient
• Initial Ventilator Settings
  • RR: 6-10 breaths/min
  • VT: 6-8 ml/kg (ideal body weight
  • PEEP: 0-5 cm H2O
  • FiO2: Minimum necessary to maintain O2 sat > 93%
  • Inspiratory Flow Rate: (suggest 100-120 L/min)
• Check Plateau Pressures and maintain at < 30 mm Hg
  • Plateau pressure reflects the pressure experienced by alveoli
  • Maintaining Pplat < 30 mm Hg helps to avoid alveolar damage
  • If plateau pressure is > 30 mm Hg, consider lowering the RR and VT.

Mechanical ventilation does not fix the underlying bronchoconstriction. Be sure to continue maximal medical management.

Trouble Shooting the Ventilator

• Hemodynamic instability and hypoxia after intubation and mechanical ventilation are common and life-threatening. Rapid recognition of the underlying problem and treatment are critical
• DOPES Mnemonic – describes the most common causes of instability
  • Displacement of the endotracheal tube (ETT)
    • Direct visualization with laryngoscope preferred (US confirmation another option)
  • Obstruction of the endotracheal tube
    • Pass ETT suction catheter
  • Pneumothorax (tension)
    • Lung POCUS for lung sliding
    • Empiric needle decompression or finger thoracostomy
  • Equipment failure
    • Disconnect the vent and deliver manual BVM breaths
  • Stacked Breaths
    • Forcibly exhale patient (gently push down on anterior chest wall with two hands until no further exhalation detected)

Trouble Shooting – Severe Acidemia 

• A pH < 7.15 can lead to physiologic issues
• Check plateau pressure and if < 30 mm Hg, consider increasing ventilation (increase RR/TV)
• Invasive Treatment
  • Inhaled Anesthetics (i.e. sevoflourane)
  • Veno-Venous (VV) ECMO

Take Home Points

• Consider parenteral epinephrine in patients with severe asthma exacerbations as inhaled beta agonists are unlikely to penetrate into the distal airways.
• Intravenous epinephrine is life-saving and safe when used appropriately.
• Use NIPPV and high-flow nasal cannula to appropriately pre-oxygenate patients and avoid critical desaturations during intubation.
• Use a strategy of permissive hypercapnea for mechanical ventilation to avoid breath stacking, hyperinflation and high airway pressures. Aim for plateau pressures < 30 mm Hg.
• Use the DOPES mnemonic to troubleshoot hemodynamic instability after initiation of mechanical ventilation.

Read More:

EMCrit Podcast 15: The Severe Asthmatic

EMCrit Podcast 16: Coding Asthmatic, DOPES and Finger Thoracostomy

REBELCast: The Crashing Asthmatic

References:

Pollack CV et al. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995; 26(5): 552-7. PMID: 7486361

Soroksky A et al. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003; 123: 1018-25. PMID: 12684289

Lim WJ et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2012. PMID: 23235608

Cydulka R et al. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med 1988; 17(4): 322-6. PMID: 3354935

Grandordy BM et al. The effect of intravenous phenylephrine on airway calibre in asthma. Eur Respir J. 1995;8:624-631. PMID: 7664864

Smith D et al. Intravenous epinephrine in life-threatening asthma. Ann Emerg Med 2003; 41(5): 706-711. PMID: 12712039

Putland M et al. Adverse events associated with the use of intravenous epinephrine in emergency department patients presenting with severe asthma. Ann Emerg Med 2006; 47(6): 559-564. PMID: 16713785

Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007

Goodacre S et al. Intravenous or nebulized magnesium sulphate versus standard therapy for severe acute asthma (3Mg trial): a double-blind, randomised controlled trial. Lancet Respir Med 2013; 1: 293-300. PMID: 24731521

Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58

This post was intially posted at coreem. Shared with permission. 

Lets talk about Headache in Adults!

From the Desk of Sagar Galwankar, MBBS, DNB, FACEE, MPH, Diplomat. ABEM, FRCP

• Headache is one of the common symptoms when patients come to the ED.
• Headache can be a Presenting Complaint when the patient arrives. "I got a Headache" and sometimes when patients are being evaluated at bedside for some other symptoms they can add the complaint "..and I also have an Headache"
• History takes paramount importance when a patient complains of Headache as a Primary Symptoms or a Co-Symptom as a part of a Series of Complaints.
• Always evaluate Headache keeping a 360 Degree approach. 
• Always address Headache. via your Thought process, History taking and Clinical Exam.

Vital Signs take a Lot of Importance and ask for them as you immediately prescribe pain medications to treat the PAIN.

Temperature, Pulse, Blood Pressure, Respiration, Pulse Ox, and Bedside Glucose are key stat Bedside Parameters which guide you to a story. Order an EKG Stat and read it.

Remember:  Gender does matter ! Pregnant Females & Females who do not know they are pregnant can come to the ED. Being Pregnant Changes the way you will evaluate these patients. Having abdominal pain, Hyperemesis gravidarum vaginal bleed can come with an headache and evaluating for abdominal emergencies and Ruling out Ectopic Pregnancy at the same time deciding about CT Head and Headache work up is a complex issue. They can also have HELP Syndrome or Eclampsia also can start with Headache.

• Age is crucial before Young Female with Headache and Cold and Cough is different from a 50 Year old with Headache and Blurry Vision.
• History taking should include: When did it start, how severe is it from a scale of 1-10, any other symptoms of Dizziness, Focal weakness, Gen weakness, Vision changes, neck pain, Syncope Seizures, Nausea, Vomiting Diarrhea, Chest Pain, SOB, Neck Pain/Stiffness, Dizziness, Vertigo have to be ruled in or ruled out.
• Past History of DM HTN CAD CVA Cancer HIV Hep B Hep C are important. Is patient on anticoagulants also is key history point.

Some Cluster approaches are:

• Fever, Tachycardia, Headache, Neck Pain: Here Headache can be as simple as a Viral Fever or as severe as early meningitis or even a URI if Cold Cough Sinus Tenderness are present.
• Headache could be a early Bleed (Subarachanoid) or even a CVA when patients have vasculitis, Bleeding disorders, Hypertension , DM.
• Headache can be due to Glaucoma or due to Otitis Media or even early Temporal arteritis.
• Headache can be segmental along a nerve for a early developing Zoster.
• Syncope, Fall, Seizure, Loss of Sensorium, Altered Mental Status with Headache all can be indicating a worse diagnosis  than how the Headache presented.
• Post Ictal Phase can present as Headache.
• Another confounder: MI/ACS can also present as an Headache so can arrhythmia or PE. So EKG Trop are Important.

There have been cases who have presented as an Headache and when you do labs there has been Low Hemoglobin and patient has a GI Bleed and the Immediate anemia has caused an headache.

Be very particular and alert when Patients says "Headache is what brought me to the ED". On the other hand there is tons of Literature of approach to Migraine in ED.

Its very important that you read the literature as there are various combinations of medications used to break the migraine. When a patient says "I have a Migraine attack" you still have to approach it as an HEADACHE.

Sometimes patients present with Neck Pain and Stiffness and we disregard it as "Slept on wrong side or Neck sprain". Evaluating for Cord Compression and keeping Dissection and SAH as a differential is equally important as much as ACS/MI or even a Retro pharyngeal abscess in a URI patient.

What it comes down to is:

• Vitals, Past History, Med List, Clinical Co-Symptoms, History of Complaint, Detail Clinical Exam to include total undressing of patient Neuro Vascular HFN HEENT Exam and Lab Results is crucial.
• Overdose and Drug abuse are important historical points which can indicate Cocaine abuse or even overdose unintentionally on paracetamol ibuprofen trying to self medicate with Over Counter Medications.
• CBC, LFT RFT Trop EKG UA Tox Screen and CT / MRI ESR are a part of the work up in ED.
• In a patients with Hypoglycemia or Hyperglycemia Ketoacidosis versus Toxicity v/s sepsis or infection has to be kept at back of mind.
• In HTN emergency headache can be because of raised BP and Raised BP can cause headache. Treating both is important but also is important ruling out cardiac pathologies a CT Head and look for Posterior Reversible Encephalopathy Syndrome.
• I have also read reports where patients were on anticoagulants and had neck pain and when MRI was done it has Hemomyelia into the spinal cord.
• There have been cases alcoholism where patients wake up with headache in ED but they dont know that Methanol or Toxic alcohols were also drunk and they have an Headache.
• Being very aggressive to rule out meningitis and SAH and using Spinal Taps with Clinical Co relation is important in the ED.
• Patients often return post spinal tap with headache and at this time Blood Patch becomes a choice after you have ruled out any other cause or pathology.
• Patients also have headache after Nitro given for Chest Pain.
• Fever can exacerbate Headache and Hunger can do that too.
• A TIA can be presenting as Headache being one of the Co-Symptoms.

Documentation:

• Always Document in detail the history the clinical exam and the plan for ordering tests and meds and chart your thought process and notes as you reevaluate the patient.
• That helps and maintains the continuum of care at the same time maintaining standards of care.
• Discharge is a crucial part. Here too Educating the patient and giving return instructions is key.

Do not Disregard or Less regard HEADACHE. Its a Part of the PAIN PATHOLOGIES which can cause PAIN if ignored.

Patients have Pain , treat it first but work it up and decipher the cause then treat the cause....  FOR THE PATIENTS !

Author: 

                                                   

Dr. Sagar Galwankar  

MBBS, DNB, FACEE (INDIA), MPH, Dip. ABEM (USA), FRCP (UK)

Chief Academic Officer of the INDO-US Emergency and Trauma Collaborative 

Assistant Professor 

Department of Emergency Medicine 

University of Florida, Jacksonville 

(Follow Dr. Galwankar on Twitter @SagarGalwankar)

Sorting out Gabrahat (Anxiety) ~ The Common Complaint in the ED

 Gabrahat (Anxiety) is often a common complaint with many implications.

While working in Emergency Departments in India I have been surprised with what the ultimate diagnosis was when I investigated Gabrahat.

For me Gabrahat is as vague as the Horizon and I take this complaint very seriously. It is very easy for any Nurse or Emergency Physician to get framed and just label Gabrahat as Anxiety or Hysteria.

This can be the Epic Blunder of Large Proportions. 

Many times relatives who accompany the patient will Frame the Emergency Physician by saying words like “There is Tension”. What they mean to imply is Gabarahat is Stress Related.

I often relate Gabrahat to a “SENSE OF IMPENDING DOOM”. When you grade GABRAHAT in that perspective, it guides the Emergency Physician to be very Proactive and diligent.

Let me share a few blasts from the past which I have modified for the sake of Education.

Case One:

Middle Age Female comes to the ED saying that she is feeling SOB. She is hyperventilating and Diaphoretic. She says that she has been having pain all over the body and fells GABRAHAT as if something is going to happen to her.

Her vitals are stable but she continues to breathe hard and breath fast. The relatives were doing a Fine job of Framing her as hysteria.

Rapid Fire Questionnaire Labs EKG Trop and a X-ray Beta HCG UA and a BNP are ordered.

On examining the patient the only Finding is the breathing. Lorazepam given IV and Oxygen started and ABG Ordered which is showing alkalosis. Aspirin given and a bedside Glucose is Normal. She settles down but continues to breathe hard. A CTA Chest is ordered. 

There are massive shower Pulmonary Emboli. Pt gets thrombolyzed and goes to ICU.

Case Two:

A 55-year-old women comes with GABRAHAT. She says that she is afraid something is going to happen. She has no other symptom. She has no Past Psyc Issues.

Labs EKG Trop and an X-ray UA ordered. She has had a prior hysterectomy.

She had an ST Elevation MI. Went to the Cath Lab. No Symptoms at all. No Past History at all.

Case Three:

30-Year-old man came saying He had Gabrahat and felt that there was Irritation in the Chest. NO PAIN BUT ONLY IRRITATION. Exam Past History negative.

Cardiac labs CBC RFT LFT was negative so was his EKG and Xray. Against the will of the Internal Medicine Colleagues Pt admitted. 4 hour repeat EKG and Trop was placed from the ED. His EKG was normal but his Trop had become positive.

Cardiology who scheduled the patient for a cath after admitting him to CCU found a Tight Lcx Lesion which needed a Stent.

Case Four:

48 Female with Gabrahat. Second visit after discharge from the hospital. Come back saying she is afraid. No Pain, No Focus of Infection. 

CBC RFT LFT Cardiac Labs X-ray Beta HCG and UA Negative.

Says her Mind tell her Something is wrong. She has GABRAHAT.

Was admitted in a nursing home. CBC Electrolytes creatinine and SGPT was done and after overnight IV Fluids patients sent home. A CT Head done and the patient had SAH. No Neck stiffness no Eye signs. Admitted to Neurosciences ICU

The only thing that prompted a CT Head was “My Mind is telling Me. This was perceived as Hallucinations hence CT Head Ordered.

Case Five:

18 Year Old Male comes with Gabrahat with Hallucinations. He was at friends party and says “ I have gabrahat as I see a ghost”.

Tox Work up was done and it was positive for multiple substances.

Routine CBC RFT LFT EKG Trop UA and Xray with a CT Head and Tox Screen were done.

Case Six:

40 year old male comes saying that he has Gabrahat and he feels like a huge Log of wood just fell on his head and nailed his whole body vertically into the ground. Clinical Exam and Vitals were normal.

CBC LFT RFT Trop EKG Xray negative

No Neck stiffness Neuro exam normal. He kept saying I am afraid I am sinking into the ground.

CTA Aortagram ordered: He had a dissection from Thorax to iliac bifurcation.

Admitted to CVTS Sx.

Summary:

• Basic Approach should be T/P/R/BP/Pulse Ox
• I always order a CBC LFT RFT EKG Trop CXR. Looking for Rhythm abnormalities is also important. Fever can also cause Gabrahat.
• In Females in the Pregnancy Age group a HCG-UA is ordered
• If Patient has SOB I will R/O Thoracic Causes like Dissection/Pneumothorax and PE.
• If Patient has a presentation of Altered Mental Status I always order a CT Head.
• If Toxicology screen is available, I will order one.
• Co-Symptoms should guide further investigations.
• Discussing with the Relatives in key to educate them- that this is not Hysteria / Tension / Stress. Those are the diagnosis to be considered once Major Life threatening causes are ruled out.
• I have often Seen Marital Discord / Intimate Partner Abuse to be causes of GABRAHAT. So Going deeper into the history. Sitting with the patient with Privacy is the key.
• Anxiety / Panic attack also can be on the differential once Major causes are ruled out.
• Being a Compassionate Emergency Physician is the key. Communication is the answer and Competency to Care is crucial.
• GABRAHAT CAN KILL !

I want to Share a Web Review of what Non EM Experts say about GABRAHAT.

I feel a Well Trained Emergency Physician leaves no stone unturned to do the best for his/her patient

Web Review:

• http://bhj.org.in/journal/special_issue_tb/DPII_11.HTM
• http://hrelate.com/natural-remedies-for-anxiety/
• http://www.njhonline.com/1993/july_aug_93_vol_11_no_4/spider/ghabrahat.shtml

Author:

Dr. Sagar Galwankar

CEO of INDUSEM & Faculty of Emergency Medicine at University of Florida Jacksonville, Florida

@SagarGalwankar

Sagar completed his med school from the University of Pune (India). He attained Board Certified in Internal Medicine from the National Board of Examinations in India. Following this, he went on to train at the University of South Florida, USA in areas of International Health Diplomacy, Infectious Diseases and Emergency Medicine. He also holds a MPH from the University of South Florida and is a Board Certified Emergency Physician with the American Board of Emergency Medicine.

Sagar's academic and clinical career spans over a decade with experience in Education, Care and Research both in India and the USA. He has extensively published, cited and honoured for his works in International Medicine, Public Health, Infectious Diseases, Emergency Medicine and Injury Sciences. Sagar is the Founder and CEO of the INDO-US Academic Initiative for Emergency and Trauma and continue to play a defining role in establishing Emergency Medicine as a separate specialty in India.

He has had previous appointments at the University of South Florida and University of Florida in Departments of Emergency Medicine, Internal Medicine, Global Health and Mental Health. His areas of Interest include Emergency Medical Intelligence, Health Policy, Injury Medicine, International Health, Humanitarian Assistance, Quality Health Care Delivery in Emerging Economies and Global Health Diplomacy.  Sagar believes that "The role of the World's Largest and the Oldest Democracies namely India and United States is crucial for the future progress of transitional Economies and Peace across the Globe". Health is Definately an important part of this growth Story.

Originally published at beepers365.blogspot  on 11 December, 2016. Reposted with permission.