Department of Medicine: Morbidity & Mortality Conference

Department of Medicine: Morbidity & Mortality Conference
Drs. Lena Virasch, Ronak Parikh, Eileen Gajo, Katie Kaplar, Jacob (Jake) Oberwetter, Neil Panchal, Keith Smart, Anthony (Tony) Scavone

Objectives Articulate the management of Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) and corresponding sodium levels causing neurologic manifestations List the presentation and appropriate diagnostics for urinary tract infections in elderly Describe the presentation of temporal lobe strokes and its mimickers Verbalize the approach to appropriate identification of cognitive biases in medical decision making

History of Present Illness
81 y/o F with HTN and DM2 presents with confusion Patient has expressive aphasia, cannot provide meaningful history Lives at independent living section of nursing home Per nursing home clinic, patient was “not feeling well” and “is confused” Had one watery bowel movement PTA Febrile to prior to arrival per nursing home clinic Unknown when patient was last normal Per son – baseline is A&O x 3, no issues with mentation

Further History PMH: HPI + PVD
Medications: Hydrochlorothiazide, lisinopril, felodipine, cilostazol, Lantus, metformin

Emergency Dept. Examination
T 99.3, HR 105, RR 18, SpO2 88% on RA, BP 144/73 Gen: Confused, unable to provide history Neck: Supple HEENT: PERRLA, Atraumatic Lungs: CTAB Heart: Regular, equal pulses Abd: Soft, non-distended, + bowel sounds Ext: No edema Neuro: Alert & Oriented x 3. Expressive aphasia. CN 2-12 intact, DTR 2+ bilaterally, 5/5 strength bilaterally

Labs Diff: 80% PMNs No bands Urinalysis: wnl Lactate: 2.2 TSH 1.1

Imaging CT Head w/o contrast: No acute CVA/bleed
Chest Xray: Increased interstitial markings EKG: Sinus tachycardia with PACs and PVCs

Initial Floor Evaluation
Now A&O x 1 (self) Continued expressive aphasia, less alert Repeat sodium 122 (s/p 1L NS infusion) Euvolemic on exam Serum Osm 264, Urine Na 70, Urine Osm 698  SIADH Concern: Na  confusion  transferred to ICU for hypertonic saline

Syndrome of inappropriate antidiuretic hormone
Eileen Gajo, Neil Panchal Syndrome of inappropriate antidiuretic hormone

The questions Does ischemic stroke cause hyponatremia/SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)? Does the resultant hyponatremia explain our patient’s AMS?

What does ADH do? Normalizes plasma osmolality (1⁰ trigger)
free water absorption when volume (2⁰ trigger) SIADH Inappropriate free water absorption while OSM are nl/low and volume is nl (pt. euvolemic)  hypo-osmolality and hyponatremia

How does it do it?

Prevalence of hyponatremia: 12%
35% SIADH in 24%

Nervous System Disorders
Causes Nervous System Disorders Neoplastic Pulmonary Disorders Drugs Miscellaneous Acute psychosis Brain abscess Cavernous sinus thrombosis Cerebrovascular accident/Stroke Delirium tremens Encephalitis (viral or bacterial) Epilepsy GBS Head trauma Herpes zoster Hydrocephalus Hypoxic ischemic encephalopathy Meningitis Multiple sclerosis Schizophrenia SAH Subdural hematoma Wernicke encephalopathy Non Small Cell Lung cancer Pancreatic Colon Cervical Bladder Prostate Other - Brain tumors, carcinoid tumors, Ewing sarcoma, leukemia, lymphoma, nasopharyngeal carcinoma, neuroblastoma (olfactory), and thymoma Acute respiratory failure Aspergillosis (cavitary lesions) Atelectasis COPD Cystic fibrosis Emphysema Empyema Pneumonia (viral, bacterial [mycoplasmal], fungal) Pneumothorax Pulmonary abscess Pulmonary fibrosis Sarcoidosis Tuberculosis This list is exhaustive. SIADH is a known adverse effect of multiple psychotropic medications. Many therapeutic medications cause nausea, which is a powerful stimulus of vasopressin secretion. Giant cell arteritis HIV infection Lupus Idiopathic

Clinical Presentation
Serum [Na+] mEq/L mEq/L <120 mEq/L Asymptomatic Headache Nausea Vomiting Fatigue Confusion Muscle cramps Depressed reflexes Malaise Unsteadiness Restlessness Lethargy Seizures Brain-stem herniation Respiratory arrest Death Confusion usually when Na <115 mEq/L1  never happened for our pt. 1Ellis, S. J. "Severe Hyponatraemia: Complications and Treatment." QJM : Monthly Journal of the Association of Physicians. U.S. National Library of Medicine, Dec Web. 29 Mar. 2017

Treatment Depends on: 1st line: Restrict fluid (< 800 mL/day)
Degree of symptoms If acute (<48 h) 1st line: Restrict fluid (< 800 mL/day) 2nd line: Low-dose loop diuretic and oral NaCl Optimal correction: < 9 mEq/L in 24 hours Initially 4-6 mEq/L in first 2 hours if patient has severe sx. (e.g. seizures)

Hypertonic saline Severe symptoms
Raise Na quickly to prevent irreversible neurologic injury Process: IV bolus of 100 mL hypertonic saline If symptoms persist/worsen, repeat 1-2 x at 10-min intervals

Our patient Presented with altered mental status
Attributed initially to hyponatremia Although possible, unlikely given data presented Na 123 on admission  given hypertonic saline several times Despite improvement of Na to 131, NO improvement in AMS/confusion

ICU Course – Hospital Day # 2
Neurology evaluation Mild dysarthria Follow commands, but answer questions with paraphasic errors Transcortical aphasia Presumed secondary to inferior temporal lobe stroke Presumed not due to hyponatremia CTA head and carotid duplex ordered MRI not felt to be necessary at the time (unclear why) Paraphasia: Unintended syllables, words, or phrases during effort to speak Transcortical aphasia – damage to the temporal lobe, resulting in symptoms such as poor auditory compression, speech with semantic paraphasias Fundamental question: Initially patient was admitted to the ICU for altered mentation thought to be secondary to hyponatremia. Is there data to suggest sodium levels that would show this neurologic dysfunction?

ICU Course – Hospital Day # 2
Nephrology evaluation Urine studies c/w inappropriate ADH Na to 126 s/p hypertonic saline  No significant improvement in mentation Altered mentation out of context to sodium level Paraphasia: Unintended syllables, words, or phrases during effort to speak Transcortical aphasia – damage to the temporal lobe, resulting in symptoms such as poor auditory compression, speech with semantic paraphasias Fundamental question: Initially patient was admitted to the ICU for altered mentation thought to be secondary to hyponatremia. Is there data to suggest sodium levels that would show this neurologic dysfunction?

ICU Course – Hospital Day #3-4
Continued expressive aphasia and paraphasic errors with dysarthria Oriented to self only Attempts to answer but words are jumbled Repeats "this one is a B.... And this one is a C" when prompting her to name objects or answer certain questions irrelevant to alphabet Able to repeat and read words and sentences Unable to write a sentence, instead writing "A" repeatedly then writing "B" repeatedly Stroke work up Carotid dopplers and echocardiogram w/o significant abnormalities CTA head/neck: short segment stenosis into division of left MCA No abnormalities seen consistent with patient presentation

ICU Course – Hospital Day #5
MRI brain w/o contrast “Although there is artifact in the region the findings are suspicious for acute infarction in the inferior temporal lobe with involvement of the medial temporal lobe, insula and temporal operculum. Although less likely a similar appearance may be seen with herpes encephalitis and clinical correlation is advised.” Mental status stable – continued management for suspected stroke Became tachycardic to s CXR without infiltrate Lower extremity dopplers negative Spikes first fever of hospitalization (102.6) Blood cultures obtained Unclear source for fever

Decline in neurological status More lethargic No longer answering any questions or following any commands Repeat CT head “Acute infarct involving the left temporal lobe and insula as seen on recent MRI. No significant mass effect or midline shift. No acute intracranial hemorrhage.” Persistent fevers up to 103 and hypotension to 80-90s Urinalysis with positive nitrites, 2+ bacteria, no leuk est or WBCs Urine culture obtained Vancomycin/Zosyn empirically started

More alert, but continued aphasia Does not say name, age, month or place Attempts to speak and write but is word salad Does not follow commands Fever curve downtrends: One spike to 101.1 Blood pressure stabilizes Mild hyponatremia - stable at 131 Etiology of suspected stroke remains unclear

Neurologic status stable Fevers, tachycardia, hypotension – resolved Urine culture returned positive E. Coli 10-50,000 cfu/ml, pan-susceptible UTI thought to be possible source of infection Vancomycin/Zosyn dc’d, ceftriaxone started Transferred to the general medical floor Signout given with presumed stroke and UTI

Urinary Tract Infections (UTI) in the Elderly
Katie Kaplar, Anthony Scavone Urinary Tract Infections (UTI) in the Elderly

Clinical Questions What differentiates UTI from asymptomatic bacteriuria (ASB)? Does the number of colony forming units (CFU) impact threshold to diagnose/treat? Was UTI a reasonable explanation for our patient’s fever?

Background UTI is the most commonly diagnosed infection in older adults ASB also common in elderly females; rates by hospitalization and catheterization UTI + ASB  most common reason for abx. in nursing home Older patients  atypical symptoms***  UTI or ASB?  overdiagnosis, overtreatment Overutilization of abx  Clostridium difficile and Multi-drug resistant organisms

Definitions ASB  >105 CFU/mL X 2 in pts. w/o symptoms of UTI
NO abx. needed UTI  Symptoms of UTI + laboratory data confirming diagnosis Bacteria >105 CFU/mL + >10 WBC/HPF

UTI in Our Patient Symptoms UA & culture Tachycardia Fever
Word finding difficulty (i.e. AMS) Eventual hypotension …Septic UA + Nitrites 2+ bacteria (-) leukocyte esterase Culture 10,000-50,000 CFU/mL (i.e. <105) Pan-sensitive E. coli

Urine Culture Commonly used criterion to define significant bacteriuria: > 105 CFU/mL Necessary to diagnose in inpatient setting 30-50% pts. with UTI  < 105 CFU/mL If culture obtained via suprapubic aspirate or catheterization  > 102 CFU/mL OK for diagnosis

Our Patient Despite bland UA, culture > 104 CFU + AMS and fever…? UTI since unclear if pt had sx. + urine cx, neg CXR, LE dopplers and blood cx., fever after abx  conclusion  UTI as source for sepsis***

Floor Course – Hospital Day #9
EEG – sharp waves in temporal region, no epileptiform activity Recurrence of fevers – 100.8 Tachycardic to 150s Neurologic status worse: Less interactive, more delirious Unable to state name Unable to comprehend verbal or written commands Given persistence of fevers with profound aphasia, lumbar puncture obtained – day 9

Floor Course – Hospital Day #10
Continued fevers (102.7) CSF studies Glucose 142 () Protein 120 () Nucleated cells 133 () Lymphocyte predominance 91% () Concern: viral/autoimmune/fungal encephalitis Acyclovir empirically started ID consulted levetiracetam started for sharp waves noted on EEG, even in absence of epileptiform activity Later that day…

HSV-1 PCR +  HSV ENCEPHALITIS

Fever Curve Acyclovir UA/UCx Blood Cultures Lumbar Puncture
HD 3 HD 5 HD 6 HD 8 HD 9 HD 10 Acyclovir UA/UCx Blood Cultures Lumbar Puncture CXR/LE dopplers Antibiotics Pan-S Ecoli UCx

Temporal lobe stroke & HSV encephalitis
Jacob Oberwetter, Keith Smart Verbalize why this pertains to our patient Temporal lobe stroke & HSV encephalitis

The questions: How do temporal lobe strokes and HSV encephalitis present? How can you tell them apart?

Stroke ~800,000 people in US/yr
Fever  60.8% of strokes (57.6% infectious) Temporal lobe  processing sensory input (auditory, visual), language recognition/perception, and new memories Symptoms: Wernicke’s aphasia -- “word salad” Anomic aphasia – word retrieval failure Impaired verbal memory Visual changes, hallucinations (either side) L temporal lobe stroke – which our patient had Add incidence of temporal lobe stroke and incidence of fevers

HSV Encephalitis Incidence: 1:250,000; 10-20% of annual viral encephalitis cases High mortality: 20% if treated, 70% if untreated

Clinical presentation: HSV Encephalitis
Acute findings: AMS, cranial nerve deficits, hemiparesis, dysphasia, aphasia, ataxia, focal seizures >90%  1+ sx. & fever Later findings: comprehension, memory, emotional control Paraphasic spontaneous speech

Diagnosis of HSV Encephalitis
CSF PCR Sn/Sp  98%/94-100% Detectable up to 4 weeks Imaging Temporal lobe abnormalities: strong evidence for HSV encephalitis MRI ideal, CT only ~50% sensitive EEG findings: >80% of cases -- nonspecific

HSV Encephalitis Vs. Temporal Lobe CVA
Our patient… AMS, decreased comprehension Aphasia Fever Hyponatremia MRI/EEG with temporal lobe findings Add incidence of temporal lobe stroke in general. Add incidence of fevers in ischemic stroke.

Floor Course – Remainder of Hospitalization
Continuous EEG Right temporal slowing and PLEDs (Previously noted on left) C/w HSV encephalitis Repeat MRI brain Acute L temporal lobe hematoma Progression of L temporal lobe inflammation New hyperintensity of R medial temporal lobe  bilateral HSV encephalitis Continued on levetiracetam and acyclovir periodic lateralized epileptiform discharges (PLEDs)

Remainder of Hospitalization
Patient’s alertness, arousal, and level of interaction improved Able to state name, repeat words, follow commands Still with significant expressive aphasia Repeat EEG without epileptiform activity Discharged to rehab Commands – follow

Case Analysis Was there an adverse event?
Adverse event: “An unintentional, definable injury that was the result of medical management and not a disease process.” Neurologic impairment in our patient: Adverse effect secondary to delay in diagnosis? Outcome Scale Good recovery, allowing independent life without any neurological impairment Mild disability, defined by the presence of minimal cognitive alterations (speech disturbances, memory, or attention impairment and/or seizures (partially controlled with antiepileptic drugs) without consequences for socioprofessional life Moderate disability, defined by criteria identical to those of group II but with consequences for socioprofessional life Severe disability, defined by loss of autonomy requiring institutionalization or constant life aid Death Pierluissi, E, et al. Discussion of Medical Errors in Morbidity and Mortality Conferences. JAMA. 2003;290: Raschilas, F., et al. Outcome of and Prognostic Factors for Herpes Simplex Encephalitis in Adult Patients: Results of a Multicenter Study. CID. 2002;35:

Case Analysis Retrospective multicenter study of 93 patients with HSV encephalitis 6 month follow up: 35%: poor outcome (death or severe disability) 65%: favorable outcome 2 factors led to poor outcomes Simplified acute physiology score II > 27 at admission Delay of > 2 days between hospital admission and acyclovir initiation: our delay  10 days Outcome Scale Good recovery, allowing independent life without any neurological impairment Mild disability, defined by the presence of minimal cognitive alterations (speech disturbances, memory, or attention impairment and/or seizures (partially controlled with antiepileptic drugs) without consequences for socioprofessional life Moderate disability, defined by criteria identical to those of group II but with consequences for socioprofessional life Severe disability, defined by loss of autonomy requiring institutionalization or constant life aid Death Pierluissi, E, et al. Discussion of Medical Errors in Morbidity and Mortality Conferences. JAMA. 2003;290: Raschilas, F., et al. Outcome of and Prognostic Factors for Herpes Simplex Encephalitis in Adult Patients: Results of a Multicenter Study. CID. 2002;35:

Cognitive bias influencing medical decisions
Lena Virasch Cognitive bias influencing medical decisions

Overview A large systematic review of autopsy-based diagnostic errors published in 2003 estimated rate of major errors occurring 8.4% up to 24.4% Factors that can affect the prevalence of diagnostic errors include initial empiric treatments, vague symptoms, and atypical presentations of diseases Cognitive steps involved in diagnosis Perception - determining the abnormalities of physical findings and studies obtained Hypothesis generation Data interpretation/hypothesis testing - adjustment of initial hypothesis Verification

Types of Bias Premature closure Example from our case
Tendency to favor the initial hypothesis and stop searching for other possibilities One study with medical trainees instructed about the pitfalls of premature closure had more accurate diagnoses than their peers who did not have such instruction Example from our case Diagnosis of stroke made on Day 2 Initial hypothesis was maintained until LP on Day 9 Other diagnoses were not considered until fevers persisted on antibiotics

Types of Bias Anchoring Example from our case
Tendency to lock onto salient features of patient’s presentation too early on Not adjusting the initial impression in light of information obtained later Example from our case Febrile on day 5 Continued to anchor to stroke diagnosis instead of re-evaluating initial diagnosis

Types of Bias Framing effect Example from our case
Being strongly influenced by the way a case/problem is framed in how we perceive it Example from our case Presumed diagnosis of UTI made on Day 8 Transferred to floor same day Patient signed out with presumption that recent fevers were secondary to UTI This affects how accepting team perceives recent fevers and their management going forward

Types of Cognitive Biases
Confirmation bias Tendency to look for confirming evidence to support a diagnosis instead of looking for evidence to refute it Example from our case MRI: suspicious for acute infarct but mentioned differential of HSV Used MRI to confirm running diagnosis of stroke rather than considering alternatives

Availability Judging something as being more likely when it readily comes to mind, so that if a disease is not seen in a long time it may be underdiagnosed Example from our case Expressive aphasia is frequently associated with stroke Fevers in hospital often seem related to urinary or pulmonary source Encephalitis is less commonly seen and may have been overlooked in the differential In differential for both aphasia and fevers

Diagnosis momentum Once a diagnostic label is attached, it has a tendency to become more locked in the longer it is carried What can start as a possibility eventually becomes ‘definite’ and all other possibilities are excluded Example from our case Multiple handoffs throughout hospitalization ER → Floor → ICU → Floor In the span of 9 days before HSV diagnosis: 6 medical residents, 4 medical attendings, 3 neurologists Each transfer may have made stroke diagnosis seem more absolute As with all admissions to the hospital, there are multiple handoffs throughout a hospitalization

Conclusions What happened to the patient?
As always, our goal of M&M is that of education and to promote a means of thinking for how we can improve as as healthcare professionals. A new way of thinking

Conclusions What did we learn? Clinical
Hyponatremia < 115 generally causes AMS/confusion Our patient never got that low Bacteria <100,000 cfu/ml can be a UTI, but fever in UTI relatively unreliable UTI was unlikely the cause of the patient’s fevers in retrospect HSV encephalitis can mimic temporal lobe stroke This was noted as a possibility on MRI, and LP was not performed even though pt had AMS and fevers As always, our goal of M&M is that of education and to promote a means of thinking for how we can improve as as healthcare professionals. A new way of thinking

Conclusions What did we learn? Systems
Cognitive biases (anchoring, premature closure, etc.) Influence of cognitive biases on medical decision making As always, our goal of M&M is that of education and to promote a means of thinking for how we can improve as as healthcare professionals. A new way of thinking

Strategies to Minimize Bias
Reflect on decision-making process and develop awareness of how bias can affect our decisions Keep an open mind and routinely consider alternative possibilities Use resources such as algorithms and practice guidelines Minimize time pressures Maintain open discussions about patients Review and seek feedback on patient outcomes

Conclusions What do we hope to accomplish?
Change in provider behavior and medical decision making by being more aware of cognitive biases Improved patient outcomes Improved physician confidence As always, our goal of M&M is that of education and to promote a means of thinking for how we can improve as as healthcare professionals. A new way of thinking

Acknowledgements Dr. Henish Bhansali Dr. Kevin Nash
Dr. Stephen Schrantz Dr. Susan Rubin Department of Internal Medicine Guests

References Pierluissi, E, et al. Discussion of Medical Errors in Morbidity and Mortality Conferences. JAMA. 2003;290: Raschilas, F., et al. Outcome of and Prognostic Factors for Herpes Simplex Encephalitis in Adult Patients: Results of a Multicenter Study. CID. 2002;35: Raschilas et al. Outcome of and Prognostic Factors for Herpes Simplex Encephalitis in Adult Patients: Results of a Multicenter Study. CID 2002:35 Whitley et al. Viral Encephalitis. A review article. New England Journal of Medicine. 1990: Vol 324, Riancho et al. Herpes simplex encephalitis: clinical presentation, neurological sequelae and new prognostic factors. Neurol Sci (2013) 34:1879–1881. Townend et al. Stroke or encephalitis? Case report. Emergency Medicine Australasia (2005) 17, 401–404. Hoffman et al. Isolated right temporal lobe stroke patients present with Geschwind Gastaut syndrome, frontal network syndrome and delusional misidentification syndromes. Behavioural Neurology 20 (2008) 83–89. Castillo etal al. Timing for Fever-Related Brain Damage in Acute Ischemic Stroke. Stroke. 1998;29: Myron et al. Combating Hyperthermia in Acute Stroke A Significant Clinical Concern. Stroke 1998;29: Saini et al. Effect of Hyperthermia on Prognosis After Acute Ischemic Stroke. Stroke 2009;40: The Importance of Cognitive Errors in Diagnosis and Strategies to Minimize Them. Acad. Med. 2003;78:775–780. Reducing Diagnostic Errors in Medicine: What's the Goal? Acad. Med. 2002;77: An elderly woman with ‘heart failure’: Cognitive biases and diagnostic error. Cleveland Clinic Journal of Medicine November;82(11):

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