Management of the Hospitalized Patient Nephrology Cases Kerry C. - - PDF document

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Management of the Hospitalized Patient Nephrology Cases

Kerry C. Cho, MD Associate Professor of Clinical Medicine Fellowship Program Director Division of Nephrology October 16, 2015

Case 1: Hyponatremia

HPI: 49 yo M without significant medical hx had minor MVA 2 weeks prior to admission. He was the restrained passenger of a car when his car was rear-ended by another car. He had mild

• ccipital trauma and brief LOC for an unclear duration, possibly
• minutes. At an OSH, he was evaluated, head CT was negative,

and he discharged home with Norco, Flexeril, and Naproxen. Over the next two weeks, he had progressive nausea, vomiting, headaches, confusion, and difficulty concentrating. He came to ED at UCSF for evaluation.

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Case 1, continued

• Temp 36.9°, Pulse 71, Resp 16, 135/93, O2 sat 98% RA, Wt 80 kg
• Nystagmus with bilateral lateral gaze
• Lateral chest wall contusions from seat belt

Labs 118 86 13 glucose 94 serum osms 259 4.5 22 0.72 AG 10 LFT, TSH, cortisol negative Urine Na 99, Urine K 53 UA trace ketones Physical examination

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Case 1, continued

• Given 1 L normal saline in ED, Na decreased from 118 to 117
• Repeat Head CT negative

Admitted to medicine service

• Initiated on 3% hypertonic saline at 40 mL/hour, free water

restricted

• Na corrected to 125 mEq/L, HTS d/c, Na dropped to 120.
• I/O not adequately recorded
• Nephrology consulted for persistent hyponatremia
• Neurology consulted for nystagmus

ED Course

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What is 0.9% and 3% Saline?

• 154 mEq/L of NaCl
• 0.9% = 0.9 g/dL = 0.9 g per 100 mL = 9 g/L
• 2 gram per day Na diet = 5 grams NaCl

Hypertonic Saline

• 513 mEq/L of NaCl
• 3% = 3 g/dL = 3 g per 100 mL = 30 g/L

Normal Saline

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Basic Nephrology for Hospitalists

• EFWC = Urine Flow x [1 – (UNa + UK/PNa)]

where UNa + UK are urine concentrations, and PNa is plasma [Na] Implications of (UNa + UK) > PNa

• Free water restriction will not work
• Hypertonic saline will likely be necessary to prevent desalination

with retention of free water

• Consider nephrology consultation

Electrolyte Free Water Clearance (EFWC)

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“Safe” Serum Sodium Correction

Symptomatic/severe hyponatremia  FAST correction

• Raise serum Na 4-6 mEq/L within 6 hours
• Consider 3% HTS bolus 50-100 mL IV
• Goal correction rate: 4-6 mEq/L and ≤ 8 mEq/L over any 24 hour

period Chronic severe hyponatremia with mild/moderate symptoms: SLOW

• HTS AND desmopressin 1-2 mcg IV/SQ q 8 hrs for 24 to 48 hours*
• Desmopressin prevents unanticipated water diuresis from

reversible cause of ADH release. Contraindicated in patients who cannot adhere to water restriction Fast and Slow correction

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General Advice for Hypertonic Saline in Hyponatremia Mgmt

• Rule of thumb: HTS infusion rate is typically <0.5 mL/kg/hour
• If > 0.5 mL/kg/hour, then you either made a mathematical error or

you’re correcting the serum Na too quickly.

• Consider nephrology consultation

Severe Symptomatic Hyponatremia

• Na < 120 mEq/L typically acute (< 48 hours) OR hyponatremic

patients who cannot tolerate increased ICP

• 3% HTS 100 mL IV q 10 mins prn, up to 2-3 total doses
• Goal: rapid correction of hyponatremia by 4-6 mEq/L

Hypertonic Saline

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Treatment of Osmotic Demyelination or Na Correction Rate > 8 mEq/L per 24 hr

• D5W at 6 mL/kg lean body weight IV over two hours, repeat prn
• Desmopressin 2 mcg IV/SQ q 6 hours
• Goal: drop serum Na by 1 mEq/L per hour to original target Na
• Example: Initial Na 110 mEq/L, original goal Na 116 mEq/L,

actual Na 125 mEq/L.

• Treatment with D5W and desmopressin should return Na to 116

mEq/L over about 8-10 hours

• Limitations: rat model, case reports in humans; ideal goal Na and

rate of correction undefined.

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Hospital Course, continued

• 3% Hypertonic restarted at 40 mL/hour, Na checks q 2-3 hours
• Na reached 125 mEq/L, 3% HTS d/c, Na returned to 120 with next

lab draw

• Urine output never adequately recorded
• Pt insistent that free water restriction followed

Nystagmus

• Labyrinthine dysfunction given +head thrust to R and gaze evoked

nystagmus to L, probable labyrinthine concussion

• Hyponatremia likely related to TBI, recommended MRI

Hyponatremia

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Hospital Course, continued

• Multiple areas susceptibility in the left occipital lobe, likely due to

age indeterminate microhemorrhages, possibly traumatic. With recurrent hyponatremia off HTS, tolvaptan 15 mg PO given

• nce
• Na corrected 6-8 mEq/L over first 24 hours
• Second dose of tolvaptan 15 mg the following day, observed
• vernight then discharged.
• Required 2-3 additional doses of tolvaptan over next two weeks at
• utpatient
• Na normalized on labs 2, 3, and 6 weeks post-discharge

Brain MR

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ADH receptor antagonists: Vaptans

• V1a - vasoconstriction
• V1b - ACTH release
• V2 - antidiuretic response

Vaptans – ADH receptor antagonists

• V2R specific: tolvaptan, mozavaptan, satavaptan, and lixivaptan

(only tolvaptan available in the US)

• Conivaptan: V2 and V1a antagonist, IV formulation, available in US
• True aquaretics/diuretics, not natriuretics: free water loss with

neutral effect on Na balance Three receptors for vasopressin/ADH

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Tolvaptan Information

• 15 and 30 mg tablets available in US
• Tablets > 30 mg available outside US; 45, 60, and 90 mg tablets
• Not approved for usage in symptomatic/severe hyponatremia
• Poorly tolerated chronically due to aquaresis, nocturia, thirst, dry

mouth

• Limited data on clinical outcomes and long term outcomes
• May result in overrapid correction of serum Na, especially if used

inappropriately. Dosages, Indications and Adverse Effects

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Tolvaptan Information

• Should not be used for longer than 30 days
• Contraindicated in patients with liver disease (including cirrhosis)
• Higher incidence of increased AST and ALT (0.9% in tolvaptan

group vs. 0.4% in placebo group) in Tempo 3:4 ADPKD trial, NEJM 2012;367(25):2407. FDA Warning

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Practical Advice on Vaptans

• Start with tolvaptan 15 mg PO x 1, first dose during daytime
• D/C exogenous sources of Na (NaCl tablets, normal saline,

hypertonic saline)

• D/C free water restriction: thirst and access to free water protect

against overly rapid correction of serum [Na]

• Repeat serum [Na] within 4-6 hours of first dose
• Onset of action 2-4 hours, peak action 4-8 hours
• Expensive (list price $400 per tablet)
• Consider nephrology consultation

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Teaching Points

• MVA and traumatic brain injury  hyponatremia
• (UNa + UK) > PNa  Free water restriction will not be effective,

consider hypertonic saline

• Consider nephrology consultation if you are considering hypertonic

saline, ddAVP, or tolvaptan use

• Tolvaptan: Stop exogenous Na intake and free water restriction,

monitor serum Na closely

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Case 2

Reason for Consultation: increased osmolar gap 62 yo WM hx morbid obesity, OSA, CHF presents with several year hx of malaise, weakness, dizziness, and head/hand tremor

• ver the last several years, worsening over the last few weeks.

He is a difficult historian with inappropriate affect, delusions, grandiosity, and confabulation.

Case 2

Medical History

• Morbid obesity
• Obstructive sleep apnea
• Congestive heart failure
• Atrial fibrillation
• Parathyroid carcinoma s/p PTX
• Kidney stones
• CKD, creatinine 2.0-2.6
• Hypothyroidism

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Case 2, continued

Medications Allergies:

• KCl 8 mEq day

Cefazolin

• HCTZ 25 mg daily

Dilantin

• Amiodarone 200 mg daily

PCN

• Synthroid 125 mcg daily
• Metoprolol 100 mg daily
• Furosemide 20 mg daily
• Atorvastatin 10 mg daily
• Coumadin
• Vitamin C

Case 2, continued

Family Hx: Non-contributory Social Hx

• Lives at home with a friend, formerly homeless.
• Worked for the British Royal Family
• Doctorates in criminology and business, master degree in

business administration and social psychology

• Former UC Berkeley professor

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Case 2,

Health-related behaviors

• Former smoker with 7 pack-years
• No EtOH or drugs.

Review of Systems

• Dizziness, weakness, feeling of impending doom, uneasiness,

insomnia, anhedonia, depression

Case Presentation

Physical Exam 36.5 158/92 65 18 99% RA HEENT normal Cardiac normal Chest normal Abdomen

• bese, otherwise normal

Ext trace pitting edema Skin abrasion over RLE, no rash Psych grandiosity

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Case Presentation

CBC Hb 12.8 otherwise normal LFT Normal INR 2.7 Albumin 3.5 Glucose 114 Ca/Mg/PO4 normal 142 100 17 3.3 31 2.4 Anion gap 11 Serum Osms 354  344 (normal 285-293)

Osmolar Gap

Osm Gap = Measured Osms – Estimated Osms Estimated Osms = 2Na + BUN/2.8 + Glucose/18 + Ethanol/4.6 Normal Osm Gap < 10 In this case, Estimated Osms = 2 x 142 + 17/2.8 + 114/18 = 297 Osm Gap = 354 – 297 = 57

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Quick note about units

Glucose

• Molecular weight: 180 daltons
• Measured in mg/dL
• Conversion mg/dL to mmol/L: 10 dL/L x 1 mmol/180 mg

Urea

• Molecular weight: 60 daltons
• BUN = blood urea nitrogen, concentration measured mg/dL
• Nitrogen component of urea: 2 nitrogens = 28 daltons
• Conversion mg/dL to mmol/L: 10 dL/L x 1 mmol/28 mg

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Differential Diagnosis?

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DDx: Increased Osmolar Gap

Increased Osmolar Gap AND Increased Anion Gap

• Ethylene glycol, methanol
• Formaldehyde, paraldehyde
• Diabetic and Alcoholic ketoacidosis
• ESRD without dialysis
• Lactic Acidosis

Increased Osmolar Gap with Normal Anion Gap

• Isopropanol, diethyl ether, mannitol
• Hypertriglyceridemia*, hyperparaproteinemias*

Case 2: Additional History

He reports bathing with isopropanol (isopropyl alcohol) when he was morbidly obese because it was difficult for him to get into a shower or bathtub. After losing a significant amount of weight, he continued to wash with isopropanol up to 15 times/day using 3-4 quarts/day.

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Additional Information

Urine toxin screen – negative Serum ethanol – negative Serum isopropanol – none detected Serum acetones – 166 mg/dL, roughly 28 mmol/L

Common Uses of Isopropanol

• Antifreeze
• De-icers
• Liquid detergent
• Disinfectant
• Glass cleaner
• Jewelry cleaner
• Rubbing alcohol
• Spot stain remover

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Isopropanol Ingestion

• Pediatrics – accidental ingestion
• Adults – substitute for ethanol, “blue heaven”

Toxicity 20 mL signs/symptoms intoxication 150-200 mL lethal dose

Isopropanol Pharmacology

• Orally absorbed within 2 hours
• Metabolized by liver alcohol dehydrogenase into acetone
• Kidneys - 80% excreted as acetone, 20% excreted unchanged
• Half-life 3 to 7.3 hours

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Alcohol Intoxications

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Methanol Ethanol Isopropyl Alcohol Ethylene Glycol

Fruity odor

Y Y Y N

• Met. Acid

Severe Mild N Severe

Anion gap

Large Moderate Slight Large

Osm gap

Y Y Y Y

Low glucose

N Y Y N

Metabolites

Formic acid Hydroxy- butyric Acetone Glycolic and

• xalic acids

Other

Blindness Acetoacetic acids Gastritis UGIB Crystalluria

Management: Supportive

• No role for activated charcoal or gastric lavage
• Isopropanol decreases gluconeogenesis
• Concurrent rhabdomyolysis/AKI from depressed CNS
• Fluids

Indications for Hemodialysis

• Isopropanol level > 400 mg/dL
• Respiratory failure, mechanical ventilation
• Hypotension requiring pressors

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Transdermal Absorption of Isopropanol?

Rat model of topical isopropanol absorption

• Boatman RJ et al. Drub Metab Dispos 1998;26:197-202.

Alcohol hand-rubs in hospitals

• q 10 mins x 4 hours
• Measurable serum isopropanol levels, 0.5-1.8 mg/L
• Turner P et al. J Hospital Infection 2004;56:287-90.

Hemorrhagic gastritis from alcohol rubdown for fever reduction

• Dyer S et al. Ann Pharmacother 2002;36:1733-5.

Teaching Points of Case 2

• Remember to check serum osmolarity when considering

ingestions and altered mental status

• Estimated Osmolalty: Remember conversions and BUN
• DDx of Osmolar Gap with Normal Anion Gap
• Isopropanol, diethyl ether, mannitol
• Hypertriglyceridemia*, hyperparaproteinemias*
• Methanol, ethanol, and ethylene glycol increase serum
• smolality, osmolar gap, and anion gap (with metabolic acidosis)

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Case 3

CC: acute kidney injury (case seen in 2008) 28 yo WM hx nephrolithiasis and bilateral ureteral stents. First episode of nephrolithiasis in 2002 as 22 year old. Bilateral ureteral stents were placed. Patient lost to follow-up. Returns for follow-up and found by urology to have a complete R ureteral stent and a fragmented L ureteral stent. Underwent bilateral nephrolithotomy with calcified ureteral stent removal and partial stone removal. Bilateral upper pole nephrostomy tubes inserted.

Case 3: History

Post-operative course

• Ciprofloxacin IV
• Hypoxia and respiratory failure, transferred to ICU, started on

BiPAP then intubated

• Vanco and Zosyn
• Heparin gtt for possible PE until Chest CTA negative
• LE Doppler US negative for DVT

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History

Baseline creatinine 1.2 mg/dL on admission in April and previously in February 2008 Following AM, creatinine 2.34 mg/dL with excellent urine output from nephrostomy tubes, ~ 60 mL/hour mostly from R nephrostomy tube. Medical History

• CKD, baseline creatinine 1.2 mg/dL
• HTN
• Nephrolithiasis

History

Allergies: NKDA Medications

• Dilaudid, heparin gtt, atenolol, Zosyn, vancomycin,

albuterol/atrovent Social Hx: No tobacco/EtOH/drugs Family Hx: Dad with 2 kidney stones

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History

Physical Exam T 37.3 RR 10-38 HR 70-100 BP 130-190/50-80 130.8 kg Obese Intubated RRR normal JVP, no m/r/g Decreased breath sounds L>R Bilateral nephrostomy tubes and Foley Soft nt nd +BS 1+ edema

Labs

138 104 20 WBC 14.4, Hb 11.5, Plts 312 4.4 26 2.34 Calcium 1.79 (11.2 mg/dL on admission) Mg 1.9 PO4 2.9 UA: 100 protein, large Hb, +LE Sediment: many non-dysmorphic rbcs, few granular casts

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Radiology

CXR: decreased lung volumes, moderate L pleural effusion Renal US:

• R kidney 12.6 cm, no hydro/stones, previous hydro resolved.
• L kidney 13.1 cm, grade 3 hydro, dilated calyces, mx stones

DDx

• ATN
• Obstructive nephropathy
• Hypercalcemic ARF

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Recommendations

• No acute need for IHD or CRRT
• IR to fix non-functioning L nephrostomy tube
• Aggressive hydration
• IV furosemide
• Zometa IV
• PTH, vitamin D
• Endocrinology consult

Nephrostogram

• L nephrostomy tube malpositioned
• Injection of contrast into L nephrostomy tube flowed into pleural

space with respiratory variation of urine in Foley tubing

• R nephrostomy tube: properly positioned, but no flow of injected

contrast into ureter. Next day in IR

• Bilateral ureteral stents and nephrostomy tubes
• L chest tube for pleural effusion

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Evaluation of Hypercalcemia

• 25-hydroxyvitamin D: 19 (low)
• 1,25-dihydroxyvitamin D: 47 (normal)
• PTH: 181, 989, 630
• TSH, free TF: negative
• Cortisol: normal
• Stone analysis: calcium oxalate monohydrate

Endocrinology Consult for MEN syndrome

Quick Comments about Calcium

Total Calcium Measured in mg/dL, normal range 8.8 to 10.3 mg/dL Ionized Calcium

• Measured in mmol/L, normal range 1.16 to 1.36 mmol/L

Molecular weight calcium = 40 daltons Total calcium normal range is 2.3 to 2.575 mmol/L Ionized calcium is 40-50% of total calcium

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Creatinine Arrow = bilateral nephrostomy tubes Ionized Calcium Arrow = Zometa IV

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History

Physical Exam T 37.3 RR 10-38 HR 70-100 BP 130-190/50-80 130.8 kg Obese Intubated RRR normal JVP, no m/r/g Decreased breath sounds L>R Bilateral nephrostomy tubes and Foley Soft nt nd +BS 1+ edema

Labs

138 104 20 WBC 14.4 4.4 26 2.34 Hb/Hct 11.5 34.5 Plt 312 Calcium 1.79 (11.2 mg/dL on admission) Mg 1.9 Phosphate 2.9 UA: 100 protein, large Hb, +LE Sediment: many non-dysmorphic rbcs, few granular casts

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Radiology

CXR: decreased lung volumes, small-moderate L pleural effusion Renal US:

• R kidney 12.6 cm, no hydro/stones, previous hydro resolved.
• L kidney 13.1 cm, grade 3 hydro, dilated calyces, mx stones

Anatomy for Nephrostomy Tubes

• Campbell-Walsh Urology, 9th Ed. 2007

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Teaching Points for Case 3

• Nephrostomy tubes
• Can be inserted above or below 12th rib
• Tubes over the 12th rib may enter the pleural space
• Displaced nephrostomy tubes can cause pleural effusions from

urine leaks

• Urine leak confirmed with Fluid Creatinine > Serum Creatinine
• Severe nephrolithiasis  consider primary etiology

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Drug Toxicity Case

65 yo M hx schizophrenia, gastritis, HTN, resident of board/care

• facility. Brought in by ambulance after being found down at home

with altered mental status. Noted to have slurred speech and tremulousness. Initial Evaluation: CXR normal. Brain CT negative. Medication reconciliation between caretaker and primary MD revealed that he had been taking lithium 600 mg BID instead of the prescribed 300 mg BID for unclear duration. Other medications include mirtazapine 15 mg and olanzapine 5 mg at night. Baseline creatinine 1.2 in April 2015.

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Hospital Course, continued

Physical Exam: normal vitals, afebrile, normal O2 saturation Cachectic, incoherent, slurred speech Dry MM Neuro: somnolent, not following commands, tremulousness, normal reflexes. Labs: 144 120 32 glucose 109, Ca 9.3, Mg 3.1, PO4 3.4 5.0 19 1.86 Li 4.3

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Hospital Course, continued

Lithium level 4.3, measured 12 hours after presentation to ED Nephrology and psychiatry consultation

• R femoral temporary dialysis catheter placed for urgent dialysis
• Li level prior to 1st HD 3.6, decreased to 2.0 mEq/L 8 hours after

HD

• 2nd HD treatment reduced Li level to 1.5
• 3rd HD treatment today October 16, 2015
• Urine output 3+ L/day despite minimal PO intake and hypovolemia

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Treatment of Lithium Toxicity

• Airway/Breathing/Circulation: Monitor mental status, seizures
• Hydration
• Lithium induced nephrogenic diabetes insipidus due to chronic

exposure  May require NS for hypovolemia and D5W for prevention/treatment of hypernatremia

• GI decontamination
• Activated charcoal  No role
• Whole bowel irrigation/polyethylene glycol: Large acute

ingestions or sustained release Li formulations

• Sodium polystyrene  theoretical benefit, impractical

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Lithium Toxicity: Hemodialysis

• Lithium easily dialyzed: Small, not protein bound
• Indications for hemodialysis: Unclear/controversial
• Serum [Li] > 4 mEq/L regardless of symptoms
• Serum [Li] > 2.5 mEq/L with symptoms (seizures, altered mental

status), reduced GFR from AKI or CKD that limits Li excretion

• Consider consultation with medical toxicology or poison control

center

• Nephrology consultation for hemodialysis
• Continuous renal replacement therapy (CRRT) for unstable

patients

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SILENT: Syndrome of Irreversible Lithium Effectuated Neurotoxicity

• Prolonged neurological and neuropsychological symptoms

following lithium toxicity

• Symptoms
• Cerebellar dysfunction (most common)
• Extrapyramidal symptoms, brainstem dysfunction, dementia
• Blindness, nystagmus, choreoathetoid movements, myopathy
• Symptoms can persist for months to years

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Teaching Points for Case 4

• Medication reconciliation was key to patient care
• Lithium toxicity may require consultation with medical toxicology (or

poison control), psychiatry and nephrology

• Consider hemodialysis
• Lithium level > 4 mEq/L, regardless of symptoms
• Lithium level > 2.5 mEq/L with symptoms
• Multiple HD treatments may be needed to remove lithium
• Nephrogenic diabetes inspidus from chronic lithium use may be

present and may cause polyuria, hypernatremia, hypovolemia

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