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Question and answer links
- W1: An 81-year-old man has had three days of fever and poor intake. Which single bedside finding is the most reliable eviden · Answer
- W2: A 66-year-old woman started hydrochlorothiazide 25 mg daily for hypertension six weeks ago. Which set of laboratory chan · Answer
- Q3: Mrs. Abernathy is 72 and 60 kg, with a blood pressure of 94/56 lying, a heart rate of 112, 3.5 kg below her clinic weigh · Answer
- Q4: If you were thinking hypernatremia explained solely by lack of water access, with normal urinary concentrating ability , · Answer
- Q5: After stabilization, sodium 149; urine osmolality 160 mOsm/kg before desmopressin 2 mcg IV and 172 two hours after; 30 y · Answer
- Q6: Corrected calcium 12.2 mg/dL (10.3 eight months ago), intact PTH 84 pg/mL, creatinine 2.0 and still moving, hydrochlorot · Answer
- Q7: After treatment for lithium-associated decreased consciousness, she is alert, with creatinine 1.6 (baseline 1.0), lithiu · Answer
- Q8: After recovery of this acute water-balance problem, serial measurements over several years show a sustained fall in eGFR · Answer
Session S1 · 2026-10-22 · supplementary · 20 min Anchor: Fluids, electrolytes and acid-base — hypernatremia from lithium nephrogenic diabetes insipidus, with the lithium-specific calcium point · Integrates: lithium and thiazide pharmacology, hemodynamic AKI, geriatric medication safety, IV fluid selection and the free-water deficit, hypercalcemia (recognized, not walked) One-line hook: Thirty years of lithium, a new thiazide, an over-the-counter NSAID and a flu: three of the four causes of this emergency are on the medication list.
Fictional patient. Every name, date and number in this case is invented for teaching. Self-study: about 20 minutes. Commit to an answer before you open each folded callout.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
By the end of this case the student can:
- Judge volume status in an older adult from the bedside signs, and explain which ones mislead, urine output included.
- Choose and sequence fluids for hypotensive hypernatremia, calculate the free-water deficit, and set a safe daily rate of fall.
- Read the urine osmolality against the serum sodium to recognize diabetes insipidus, and separate nephrogenic from central DI by the desmopressin response.
- Interpret a high corrected calcium against its PTH, and decide whether the emergency protocol is needed.
- Manage lithium toxicity with hemodynamic AKI: decide which drugs to hold and who decides about the lithium, and name the drugs that raise lithium levels.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
Two readiness items.
W1The sign you can trust
An 81-year-old man has had three days of fever and poor intake. Which single bedside finding is the most reliable evidence that he is volume depleted?
A dry mouth and tongue when you examine him on the early-morning ward round
Skin on the back of his hand that stays tented for several seconds after a pinch
A 22-mmHg systolic fall on standing and a 2-kg drop from his last weight
A urine output below 30 mL per hour over the last four hours of the night shift
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Orthostatic vital signs — a systolic fall of more than 20 mmHg (or diastolic more than 10) on standing — paired with a measured weight change (1 kg is about 1 L of fluid) are the most dependable bedside evidence that the circulation is short of volume. Signs built on skin and mucosa wear out with age. Why not the others: A — mouths dry from mouth breathing, oxygen and anticholinergic drugs; B — aged skin loses its recoil whatever the volume (and turgor is checked at the forearm); D — urine output falls with dryness only if the kidney can concentrate; a kidney that cannot keeps making urine while the patient dries out. Course reading: Evidence for this case
W2The thiazide signature
A 66-year-old woman started hydrochlorothiazide 25 mg daily for hypertension six weeks ago. Which set of laboratory changes is the thiazide's signature, and when should her first check have been?
Low sodium, low potassium, high calcium, high uric acid; BMP at 1–2 weeks
High sodium, low potassium, low calcium, low magnesium; a BMP at 3 months
Low sodium, high potassium, low calcium, low uric acid; a BMP at 6 months
High sodium, high potassium, high calcium, low uric acid; no routine check
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Thiazides block the sodium-chloride cotransporter in the distal convoluted tubule — the segment that dilutes urine — so they impair free-water excretion (low sodium), waste potassium and magnesium, and increase calcium reabsorption (high calcium) and uric acid retention. The first BMP (sodium, potassium, creatinine) belongs 1–2 weeks after starting or changing any diuretic, sooner and more often in older adults. Why not the others: B — low calcium is a loop diuretic's pattern, and three months misses the window; C — high potassium belongs to potassium-sparing drugs and ACE inhibitors; D — no diuretic raises sodium, potassium and calcium together, and every diuretic start gets a check. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3 · Q4
Setting: Emergency department, Dubuque, 10:40 on a Tuesday in October.
Patient: Mrs. Ruth Abernathy, 72, a retired bookkeeper, brought in by her daughter, who found her in bed this morning confused and unable to stand without help.
History of present illness: She has taken lithium for bipolar I disorder for 30 years, with no hospitalization in 25. She has always been "a big water drinker" — a jug by the bed, up twice a night. Six weeks ago her primary care clinician added hydrochlorothiazide for a blood pressure of 152/88; no blood test followed. Two weeks ago she started ibuprofen for a knee flare. Over the past week she was up five or six times a night, "drinking pitcher after pitcher," and her hands shook more; then, four days ago, a viral illness — fever, aches, sore throat — put her to bed, and she drank little. No vomiting or diarrhea.
Baseline (annual lithium visit, eight months ago): sodium 141 mEq/L, creatinine 1.0 mg/dL (eGFR 60 mL/min/1.73 m², CKD-EPI 2021), calcium 10.3 mg/dL, lithium 0.7 mEq/L, TSH normal.
Medications (pill organizer and pharmacy record):
| Drug | Dose | Route | Frequency | Indication | Started |
|---|---|---|---|---|---|
| Lithium carbonate, extended-release | 900 mg | PO | nightly | Bipolar I disorder | 30 years ago; dose unchanged for 6 years; last dose 21:00 last night |
| Hydrochlorothiazide | 25 mg | PO | daily | Hypertension | 6 weeks ago |
| Ibuprofen (OTC) | 400 mg | PO | three times daily | Knee osteoarthritis | 2 weeks ago |
| Levothyroxine | 75 mcg | PO | daily | Hypothyroidism | 8 years ago |
Vitals: T 37.6 °C · heart rate 112 lying, 126 sitting up · BP 94/56 lying, 80/50 sitting up (she cannot stand) · RR 18 · SpO₂ 96% on room air · weight 60.0 kg (clinic weight four weeks ago 63.5 kg).
Exam: Drowsy, oriented to name only, follows simple commands. Coarse tremor of both hands. Mucous membranes dry; skin turgor poor. Neck veins flat at 30°. Lungs clear. No edema. No focal weakness; neck supple. Crepitus in the right knee.
ED studies: CT head without contrast — no acute findings. ECG — sinus tachycardia 112/min, QTc 410 ms, no ectopy.
| Test (11:00) | Result | Reference range |
|---|---|---|
| Sodium | 157 mEq/L | 135–145 |
| Potassium | 3.6 mEq/L | 3.5–5.0 |
| Chloride | 118 mEq/L | 98–107 |
| Bicarbonate | 27 mEq/L | 22–28 |
| Anion gap, Na − (Cl + HCO₃) | 12 mEq/L | 8–12 |
| BUN | 44 mg/dL | 7–20 |
| Creatinine | 2.0 mg/dL (baseline 1.0) | 0.6–1.1 |
| BUN:creatinine | 22:1 | 10–20:1 |
| eGFR | not valid — creatinine is moving | — |
| Glucose | 110 mg/dL | 70–99 |
| Calcium, total | 11.9 mg/dL | 8.5–10.5 |
| Albumin | 3.6 g/dL | 3.5–5.0 |
| Serum osmolality, measured | 337 mOsm/kg | 275–295 |
| Lithium (14 h after last dose) | 1.6 mEq/L | 0.6–1.2 |
| Hemoglobin | 13.9 g/dL (12.6 eight months ago) | 12.0–16.0 |
An intact PTH and a urinalysis with urine osmolality have been sent.
Q3The first liter
Mrs. Abernathy is 72 and 60 kg, with a blood pressure of 94/56 lying, a heart rate of 112, 3.5 kg below her clinic weight, sodium 157, creatinine 2.0 (baseline 1.0) and lithium 1.6. Which fluid plan is right?
D5W at 250 mL/h to replace the full 3.3-L water deficit in about 13 hours, sodium rechecked tomorrow
A liter of 0.9% saline with reassessment now, then D5W for the deficit with a monitored, initially conservative sodium-correction plan
0.45% saline at 75 mL/h with all of her home medicines continued, sodium rechecked in the morning
Furosemide 40 mg IV with 0.9% saline to flush out the calcium and the lithium, then water by mouth
Show answer and explanation · Link to this question
Correct answer: B
Learning point: She is hypotensive with suspected AKI (creatinine twice an eight-month-old baseline, so the timing needed for formal staging is not yet established), so the circulation comes first — and to a plasma sodium of 157, 0.9% saline (154 mEq/L) is effectively isotonic: (154 − 157) ÷ (27 + 1) ≈ −0.1 mEq/L per liter. Then free water: deficit = total body water × (Na/140 − 1) = (0.45 × 60) × (157/140 − 1) = 27 × 0.121 ≈ 3.3 L, plus ongoing urine and insensible losses, given as D5W or water by mouth when safe. For hypernatremia of uncertain duration, use an initially conservative correction plan of about 10 mEq/L over 24 hours, adjust to serial sodium and ongoing losses, and avoid prolonged undercorrection. The traditional 10–12 mEq/L daily limit is not a proven universal adult safety boundary; adult observational evidence is conflicting and does not establish an optimal rate. Why not the others: A — right fluid, wrong order and pace: the whole deficit in 13 hours aims for a 17-point fall in half a day; C — too little to restore the circulation, and it keeps the three drugs that caused this; D — a loop diuretic in a dry patient deepens the deficit and the AKI. Course reading: Evidence for this case
11:30. Lithium, hydrochlorothiazide and ibuprofen are held, and toxicology/nephrology are called immediately for the neurologic findings and possible dialysis indication. A liter of 0.9% saline runs in over 45 minutes; by 12:15 her blood pressure is 108/62. D5W follows, its rate set to her measured urine output plus enough of the deficit to lower the sodium about 10 a day, with a sodium every 4 hours.
12:15 — the urine is back. Her first void in the department, at 11:05, was 400 mL of pale, clear urine: specific gravity 1.004, osmolality 160 mOsm/kg; protein, blood, glucose, leukocyte esterase and nitrite negative; microscopy bland. The ED attending's note reads: "Hypernatremia from poor intake during a viral illness — she couldn't get to water."
Q4Evidence update
Concordance-style practice: a judgment about how a finding should move your thinking, not a graded test. There is no expert panel behind the key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."
If you were thinking hypernatremia explained solely by lack of water access, with normal urinary concentrating ability, and you then learn that her urine osmolality is 160 mOsm/kg while her serum sodium is 157, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: A
Formative evidence update: The letter is a teaching anchor. Accept a justified adjacent response; this is not an expert-panel-validated score. Learning point: If no water going in were the whole story, ADH would be at full strength — her serum osmolality is 337 — and a kidney that can respond would make concentrated urine, above 600 mOsm/kg. Urine at 160 with a sodium of 157 is a kidney pouring out free water during a water deficit: diabetes insipidus. The finding counts only because it is paired with the high sodium; 160 in someone with a sodium of 138 who just drank water would be normal. What else could it mean, and what would move you: an osmotic diuresis also keeps urine flowing, but her glucose is 110 and she has had no mannitol. The illness still matters: it took away the water she needed to keep pace with a leak she already had (the jug, the nights up). Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q5 · Q6
13:00. Blood pressure has recovered to 112/64, but she remains drowsy and oriented only to name. Toxicology and nephrology treat this as possible clinically significant lithium neurotoxicity despite the serum level of 1.6. They initiate urgent hemodialysis; the neurologic indication does not depend on a high lithium threshold. The prescription and concurrent water replacement are individualized to control the sodium trajectory, with frequent sodium checks. Diagnostic testing for DI does not delay treatment.
The next morning, after extracorporeal treatment. She is awake and oriented. Sodium is 149 and lithium 0.6 after a small monitored rebound; urine output remains 150–200 mL/h despite restored perfusion. Two familiar volume clues failed her: she kept passing urine while hypotensive, and her urine was dilute although her kidneys were underperfused (prerenal urine is usually concentrated, specific gravity above 1.020). The orthostatic vitals, the 3.5-kg weight loss, the hemoglobin rise and a BUN:creatinine ratio of 22 (no bleeding, no steroids) made the volume call. FENa was not used: she is on a thiazide.
After stabilization, nephrology evaluates the persistent concentrating defect with desmopressin 2 mcg IV — synthetic ADH — at 08:00, using a fresh pre-dose urine sample. No water-deprivation test is needed or safe during this recovering water deficit. Sodium, urine output and water replacement are reassessed every 2 hours during this monitored test; desmopressin can change water handling if a response occurs.
| Test | Result | Reference range |
|---|---|---|
| Urine osmolality, day 2 at 07:45 (before desmopressin) | 160 mOsm/kg | 50–1,200 |
| Urine osmolality, day 2 at 10:00 (2 h after desmopressin) | 172 mOsm/kg | 50–1,200 |
| Sodium, day 2 at 09:30 | 149 mEq/L | 135–145 |
| Intact PTH (drawn 11:00) | 84 pg/mL | 15–65 |
Q5Which kind of DI?
After stabilization, sodium 149; urine osmolality 160 mOsm/kg before desmopressin 2 mcg IV and 172 two hours after; 30 years of lithium; thirst and night urination for years, worse this week; calcium high. What is the diagnosis?
Central diabetes insipidus — the pituitary has stopped releasing ADH; send her home on desmopressin
Primary polydipsia — decades of heavy water drinking have diluted her urine and washed out the medulla
Osmotic diuresis from the D5W — the dextrose spills into the urine and drags extra water along with it
Nephrogenic diabetes insipidus from lithium, worsened by the high calcium — the kidney ignores ADH
Show answer and explanation · Link to this question
Correct answer: D
Learning point: A rise from 160 to 172 is only 7.5%, indicating little concentrating response to desmopressin in this patient with persistent hypernatremia. Long lithium exposure strongly supports nephrogenic diabetes insipidus; hypercalcemia can further impair concentration. Response cutoffs overlap in partial disorders and chronic polyuria, so the percentage is interpreted with the clinical context rather than as an infallible binary test. Why not the others: A — complete central DI should respond substantially to desmopressin. B — primary polydipsia alone does not explain severe hypernatremia with ongoing dilute urine here; water deprivation and chronic medullary washout can complicate formal testing. C — normal glucose and very dilute urine argue against a glucose-driven osmotic diuresis. Course reading: Evidence for this case
She has lithium's early kidney effect, a concentrating defect; the late effect, chronic tubulointerstitial injury, is one reason renal function needs regular surveillance.
The calcium. Total calcium 11.9 with an albumin of 3.6: corrected calcium = 11.9 + 0.8 × (4.0 − 3.6) = 12.2 mg/dL. Eight months ago it was 10.3. She has no constipation or abdominal pain, her QT is not shortened, and her confusion already has two causes on the table — a sodium of 157 and a lithium of 1.6.
Q6The calcium
Corrected calcium 12.2 mg/dL (10.3 eight months ago), intact PTH 84 pg/mL, creatinine 2.0 and still moving, hydrochlorothiazide for six weeks, lithium for 30 years; no constipation, abdominal pain or short QT. Which interpretation and plan fit?
PTH-independent hypercalcemia — send PTHrP, SPEP with free light chains and 1,25-vitamin D for cancer
Hypercalcemia needing the emergency protocol — calcitonin now and zoledronic acid 4 mg IV today
PTH-dependent: lithium hyperparathyroidism, thiazide-unmasked — stop the thiazide, keep rehydrating
Hypercalcemia from dehydration alone — it will settle with fluids, so no follow-up calcium is needed
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The PTH is inappropriately unsuppressed for hypercalcemia, supporting a PTH-dependent process such as lithium-associated hyperparathyroidism; the thiazide may contribute. Rehydrate, hold contributing drugs and confirm calcium status, using ionized calcium if needed. Clinical severity, not a calcium cutoff alone, determines urgent escalation. Bisphosphonates are not a routine first response to this suspected mechanism; treatment choice in kidney dysfunction is individualized rather than governed by a universal ban at CrCl 30. Why not the others: A — a suppressed-PTH malignancy pathway is not the first branch here. B — immediate bisphosphonate treatment does not address the likely drug/PTH mechanism and needs a renal-informed indication. D — persistent PTH-dependent hypercalcemia needs follow-up and specialist assessment. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q7 · Q8
Day 2, after emergency treatment. Blood pressure 116/66, heart rate 92, sodium 147, creatinine 1.6 and lithium 0.6 after extracorporeal treatment and rebound monitoring. Her right knee still hurts. The ongoing medication plan is yours to reconcile with the specialist teams.
Q7The medication reconciliation
After treatment for lithium-associated decreased consciousness, she is alert, with creatinine 1.6 (baseline 1.0), lithium 0.6, sodium 147 and a painful knee. Which ongoing medication plan is right?
Stop lithium for good and start valproate tonight; continue the thiazide and the ibuprofen for her knee
Keep lithium, the thiazide and ibuprofen held; continue specialist monitoring and involve psychiatry before any restart
Give lithium at half dose to protect her mood, stop the ibuprofen, and switch the thiazide to lisinopril
Hold only the ibuprofen; keep lithium and the thiazide as they were stable; recheck levels in a week
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Keep the interacting drugs held while recovery and the long-term psychiatric plan are assessed. A lithium level back in range does not by itself establish neurologic recovery or make the old regimen safe. Earlier, her persistent decreased consciousness justified urgent extracorporeal treatment under EXTRIP recommendations regardless of the modest serum concentration. After treatment, follow serial lithium levels for rebound, electrolytes and neurologic findings with toxicology/nephrology. Psychiatry and nephrology jointly plan mood treatment and any eventual lithium restart; do not automatically restart because one level is low. Why not the others: A — a unilateral stop that keeps both drugs that raised the level; C — no lithium while toxic, and an ACE inhibitor also raises lithium and lowers GFR in a dry patient; D — the thiazide raised both her lithium and her calcium. Course reading: Evidence for this case
Q8Years later — the second lithium problem
After recovery of this acute water-balance problem, serial measurements over several years show a sustained fall in eGFR in a patient receiving long-term lithium. Which plan best addresses the chronic kidney risk?
Coordinate nephrology and psychiatry review of the trend, lithium exposure and treatment alternatives
Assume every creatinine rise is irreversible lithium injury and stop treatment without discussion
Use one therapeutic lithium level to exclude any chronic kidney effect
Increase lithium because a lower eGFR clears the drug more rapidly
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Lithium-associated concentrating defects and chronic tubulointerstitial injury are related but different problems. A sustained eGFR decline warrants evaluation for other causes and a joint renal–psychiatric risk–benefit discussion. One current lithium level does not summarize years of exposure, and abrupt unplanned psychiatric treatment changes can cause harm. Why not the others: B skips the differential and coordinated treatment planning; C confuses current level with cumulative risk; D reverses renal drug clearance. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
Toxicology and nephrology assessed her immediately. Because decreased consciousness persisted despite restored blood pressure, they initiated hemodialysis urgently and adjusted the treatment and water replacement to the hypernatremia. She became more alert during treatment. Lithium fell below 1.0, and serial measurements over the following 12 hours detected a small rebound to 0.6 without recurrent neurologic findings; the teams judged that repeat extracorporeal treatment was not needed. Sodium fell from 157 to 147 over the first 24 hours and reached 141 on day 3; she was fully oriented the next morning. Creatinine recovered from 2.0 to 1.6 and then 1.1 by day 5, and the tremor faded. Psychiatry arranged interim mood treatment and a joint renal–psychiatric review rather than automatically restarting lithium at discharge. Any later restart requires a shared risk–benefit decision, an individualized target and a level about one week after the dose change. Off the thiazide her blood pressure was 136/80; amlodipine was selected with interaction review. Acetaminophen and physical therapy covered the knee.
Three weeks later her corrected calcium was 10.7 with a PTH of 79 — still PTH-dependent: lithium-associated hyperparathyroidism, referred to endocrinology. The NDI persists; it is the lithium's. She went home with a written water plan — water within reach, drink to thirst, a same-day sodium check if she cannot keep fluids down for a day — and a lithium sick-day plan written with her psychiatrist. Her monitoring plan includes lithium levels every 3 months because of age and risk, and creatinine/eGFR, electrolytes, calcium and thyroid function at least every 6 months, more often while abnormalities persist. Recheck lithium about one week after a dose change or interacting medicine and until stable. Her calcium and PTH receive separate endocrine follow-up.
Clinical Pearl — Read the urine against the blood A sodium above 150 with a urine osmolality below 300 is the DI pattern; a dry patient whose ADH works makes urine above 600. Desmopressin then sorts the leak — central DI concentrates, nephrogenic DI does not.
Clinical Pearl — Restore circulation, then replace water with serial sodium checks In hypotensive hypernatremia, restore the circulation with 0.9% saline, then replace free water: deficit = TBW × (Na/140 − 1), TBW 0.45 × weight in an older woman, plus ongoing losses. For uncertain-duration hypernatremia, begin with a conservative correction plan of about 10 mEq/L over 24 hours and individualize it using serial sodium and ongoing losses. Adult evidence does not establish a universal optimal rate; avoid both unmonitored correction and prolonged undercorrection.
Clinical Pearl — A thiazide in a lithium patient does three things It raises the lithium level, raises the calcium, and can unmask lithium-associated hyperparathyroidism. NSAIDs and ACE inhibitors or ARBs also raise lithium levels. If any of them must start, check a lithium level within 5–7 days.
Clinical Pearl — PTH first, and let the branch decide A high corrected calcium with a PTH that is not suppressed is PTH-dependent; lithium lives on that branch, and a thiazide often unmasks it. The emergency protocol is for a calcium of 14 or more, or severe symptoms the calcium explains; a moderate calcium (12–14) with a removable cause gets fluids and the cause removed — and no bisphosphonate while clearance is under 30.
Pitfall — "She's just dehydrated from the flu" Poor intake was the trigger, not the cause. A dilute urine at a sodium of 157 says the kidney is leaking water, and a patient with NDI keeps urinating while dry — so neither urine output nor specific gravity can judge her volume.
Pitfall — Stopping lithium on your own The medical team holds lithium when it is toxic; whether, when and at what dose it returns is decided with the psychiatrist.
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-04, aki-13, aki-22, ckd-21, lytes-01, lytes-02, lytes-10, lytes-15, lytes-27, structural-20, structural-22, structural-25.