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10/26/20151
Management of the Hospitalized PatientNephrology CasesKerry C. Cho, MDAssociate Professor of Clinical MedicineFellowship Program DirectorDivision 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 occipital 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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10/26/20152
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 hyponatremicpatients 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 once
Na corrected 6-8 mEq/L over first 24 hours
Second dose of tolvaptan 15 mg the following day, observed overnight then discharged.
Required 2-3 additional doses of tolvaptan over next two weeks at outpatient
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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10/26/20157
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 tolvaptangroup 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 over 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 obese, 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 oxalic 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 osmolality, 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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CreatinineArrow = bilateral nephrostomy tubes
Ionized CalciumArrow = 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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