Solution for Case 35

(Click here to see Case 35)

Tentative Diagnosis: The tentative diagnosis is a functional pancreatic islet cell tumor (insulinoma). The classic presentation—a middle-aged dog of a predisposed breed with episodic neurologic signs related to fasting or exercise, rapid response to sugar administration, and a documented profound hypoglycemia during an event—is highly pathognomonic for this disease. This presentation fulfills Whipple's Triad.

DDx: Other causes of profound hypoglycemia in an adult dog include sepsis, severe liver failure, hypoadrenocorticism (Addison's disease), xylitol toxicity, or a large non-pancreatic tumor (paraneoplastic hypoglycemia). However, the episodic nature and the otherwise completely normal physical exam and history make these differentials much less likely.


Further Diagnostic Test(s): The diagnostic plan is to first confirm the cause of the hypoglycemia and then to stage the disease to guide treatment.

  1. Confirmation Test: The definitive diagnostic test is the paired insulin and glucose concentration performed on the blood sample taken during the hypoglycemic episode.

    • Results:

      • Glucose: 38 mg/dL (Markedly Low) [Ref: 75 - 125 mg/dL]

      • Insulin: 45 µU/mL (Inappropriately High) [Ref: 5 - 20 µU/mL]

    • Interpretation: This result is diagnostic for an insulinoma. In a healthy animal, when blood glucose is critically low, insulin secretion should be shut down (levels <5 µU/mL). The presence of a normal to high insulin level in the face of profound hypoglycemia confirms the autonomous, unregulated secretion of insulin from a tumor.

  2. Staging: To assess the extent of the disease, imaging was performed.

    • Three-View Thoracic Radiographs: No evidence of metastatic disease was found.

    • Abdominal Ultrasound: A 1.8 cm, hypoechoic nodule was identified on the right lobe of the pancreas. The medial iliac lymph nodes were noted to be enlarged and rounded, which is suspicious for metastasis.


Definitive Diagnosis: Functional Pancreatic Islet Cell Tumor (Insulinoma) with suspected regional lymph node metastasis. More information can be found at the Merck Veterinary Manual.


Treatment Plan: The treatment plan involves immediate stabilization, followed by definitive surgical intervention and a long-term medical management strategy.

  • Immediate Stabilization: Following the diagnostic blood draw, Louie was given a slow intravenous bolus of 50% dextrose, to which he responded immediately. He was then maintained on a constant rate infusion of fluids containing 2.5% dextrose to prevent further hypoglycemia.

  • Definitive Treatment: The treatment of choice is surgical.

    • Surgical Plan: The recommendation is for an exploratory laparotomy with the goal of performing a partial pancreatectomy to remove the primary tumor nodule and debulking/removing the enlarged regional lymph nodes for biopsy. The owners were counseled that surgery can be curative but that recurrence is common due to micrometastasis.

  • Long-Term Medical Management:

    • Dietary: Louie will be transitioned to a diet high in protein, fat, and complex carbohydrates, fed as 3-4 small meals throughout the day to prevent dramatic swings in blood glucose.

    • Pharmacologic: Post-operatively, or if surgery is declined, medical management will be initiated. The first-line therapy is prednisone, a corticosteroid that counteracts the effects of insulin. If clinical signs persist, a second medication like diazoxide, which directly inhibits insulin secretion from the tumor, may be added.

  • Owner Education: The owner was instructed on how to recognize early signs of a hypoglycemic episode and how to manage it at home by rubbing Karo syrup or honey on Louie's gums, followed immediately by feeding a small meal. They were advised to avoid intense exercise and prolonged fasting.

Case 35

Signalment and History: "Louie," an 8-year-old, 28 kg (62 lb) male neutered Standard Poodle, is presented for evaluation of intermittent, episodic neurologic events that have been occurring for the past three months.

The owner reports that the "spells" are becoming more frequent and severe. They typically occur in the early morning before breakfast or after a long walk. During an episode, Louie becomes acutely weak, disoriented, and stumbles as if drunk (ataxia). He will sometimes stare blankly into space, and his muscles will twitch (fasciculations). Last night, he had his first generalized seizure, which lasted about 45 seconds.

The owner provides a crucial piece of history: during the first few episodes of weakness, she panicked and rubbed some honey on his gums, and he seemed to improve dramatically within minutes. His appetite, thirst, and urination have all been normal between these events.

Physical Exam:

  • T: 101.5°F

  • P: 88 bpm

  • R: 20 bpm

  • BCS: 5/9

Louie is bright, alert, and responsive at the time of presentation. The physical examination, including a detailed neurologic exam, is completely unremarkable. He has a normal heart rate and rhythm, clear lungs, and no abnormalities on abdominal palpation. This normal presentation between episodes is a key feature of the history.

Initial Diagnostic Workup: Given the episodic nature of the signs and the owner's report of a response to sugar, Louie was admitted to the hospital for a monitored fast.

  • Four hours into the fast: Louie became quiet, weak, and started to tremble.

  • Point-of-Care Blood Glucose (AlphaTrak): A blood glucose reading was immediately taken from his ear, which registered 36 mg/dL (Profound Hypoglycemia).

  • Blood Sample Collection: As soon as the hypoglycemia was documented, a blood sample was drawn from the cephalic vein for a full CBC, serum chemistry panel, and a paired insulin-glucose concentration test before any treatment was administered.


What will be your tentative and differential diagnosis? 

What further diagnostic test(s) you will perform to confirm your diagnosis? 

What will be your treatment plan(s)?

Solution to Case 35 will be posted on Oct 10

Solution for Case 34

(Click here to see Case 34)

Tentative Diagnosis: The tentative diagnosis is Feline Hyperthyroidism. The classic signalment (older cat), hallmark history (weight loss despite polyphagia, PU/PD, hyperactivity), and cardinal physical exam findings (thin body condition, tachycardia, heart murmur, and a palpable thyroid slip) create an almost textbook presentation for this disease.

DDx: For an older cat presenting with weight loss and PU/PD, the primary differential diagnoses include Chronic Kidney Disease (CKD) and Diabetes Mellitus. Gastrointestinal disease, such as inflammatory bowel disease or lymphoma, could also cause weight loss but would not typically explain the hyperactivity and polyphagia.


Further Diagnostic Test(s): While the clinical suspicion is extremely high, a definitive diagnosis requires hormone testing.

  • Definitive Screening Test: The single most important test is a serum Total T4 (TT4) concentration.

    • Result: Jasper's serum TT4 was 9.5 µg/dL (Markedly High) [Ref: 0.8 - 4.0 µg/dL].

    • Interpretation: A TT4 level this far above the reference range in a cat with classic clinical signs is definitively diagnostic for hyperthyroidism. No further thyroid-specific testing is needed. The elevated blood pressure reading confirms concurrent systemic hypertension, a common and serious complication.


Definitive Diagnosis: Feline Hyperthyroidism with secondary systemic hypertension. For more, see the Merck Veterinary Manual.


Treatment Plan: The treatment plan involves stabilizing the patient, managing comorbidities like hypertension, and then discussing options for a permanent cure with the owner.

  • Initial Medical Stabilization:

    • Antithyroid Medication: Jasper was started on Methimazole (2.5 mg orally twice daily). This medication blocks the synthesis of new thyroid hormones and will manage the clinical signs.

    • Antihypertensive Medication: To manage the high blood pressure and protect his eyes, kidneys, and heart, Jasper was also started on Amlodipine (0.625 mg orally once daily).

  • Monitoring and Staging:

    • A recheck appointment was scheduled for 2 weeks. At this visit, his blood pressure, T4 level, and kidney values (BUN, creatinine) will be re-evaluated. It is critical to monitor kidney function, as the high blood pressure and increased metabolic rate of hyperthyroidism can increase blood flow to the kidneys, potentially "masking" underlying chronic kidney disease. Treating the hyperthyroidism may cause a decrease in this blood flow, revealing the underlying condition.

  • Discussion of Long-Term Options:

    • The owner was counseled that while methimazole is effective, it is not a cure and requires lifelong medication.

    • The gold standard treatment, Radioactive Iodine (I-131) therapy, was strongly recommended. This is a single subcutaneous injection that is curative in over 95% of cases.

    • Other definitive options, such as surgical thyroidectomy and a prescription iodine-limiting diet (Hill's y/d), were also discussed as alternatives.

Case 34

Signalment and History: "Jasper," a 13-year-old male neutered Domestic Shorthair cat, is presented for his annual exam. The owner mentions that for his age, Jasper has been unusually active lately. Over the past six months, he has lost a noticeable amount of weight despite having what the owner describes as a "ferocious" appetite. He constantly begs for food, steals food from the other cat's bowl, and has even started getting into the trash.

His water consumption has also increased, and he has been having occasional bouts of vomiting for the past few weeks. The most significant change for the owner is behavioral; Jasper has become restless and irritable. He yowls loudly at night and paces through the house, which is very uncharacteristic.

Physical Exam:

  • T: 102.8°F

  • P: 235 bpm (Tachycardia)

  • R: 40 bpm

  • BCS: 3/9 (Thin)

  • Blood Pressure (Doppler): 180 mmHg systolic [Ref: <160 mmHg]

Jasper is restless and slightly agitated during the exam. He is markedly thin, with palpable muscle wasting over his spine and hips. His hair coat is unkempt and mildly greasy.

  • Cardiovascular: A significant tachycardia is present. Auscultation reveals a Grade II/VI systolic heart murmur best heard at the left sternal border.

  • Cervical Palpation: Careful palpation of the ventral neck reveals a small, firm, pea-sized nodule that "slips" between the fingers just to the left of the trachea. This is consistent with an enlarged thyroid gland.

Initial Diagnostic Workup: A senior wellness panel was performed.

  • Complete Blood Count (CBC): A mild erythrocytosis (elevated red blood cell count) is present (PCV: 49% [Ref: 29-45%]).

  • Serum Biochemistry Profile:

    • Alanine Aminotransferase (ALT): Moderately elevated at 195 U/L [Ref: 12-130 U/L]

    • Alkaline Phosphatase (ALP): Mildly elevated at 110 U/L [Ref: 14-111 U/L]

    • Creatinine and BUN are in the high-normal range.

  • Urinalysis (Cystocentesis):

    • Urine Specific Gravity (USG): 1.025 (inadequately concentrated)

    • All other findings are unremarkable.


What will be your tentative and differential diagnosis? 

What further diagnostic test(s) you will perform to confirm your diagnosis? 

What will be your treatment plan(s)?

Solution for Case 34 will be posed on Oct 3

Solution for Case 33

(Click here to see Case 33)

Tentative Diagnosis: The tentative diagnosis is primary hypothyroidism. This condition, often called the "great imitator," fits the case perfectly. The combination of signalment (middle-aged Golden Retriever), classic metabolic signs (lethargy, mental dullness, weight gain), hallmark dermatologic signs (symmetrical non-pruritic alopecia, rat tail), and key laboratory abnormalities (hypercholesterolemia, hypertriglyceridemia, mild non-regenerative anemia) makes hypothyroidism the leading differential.


Further Diagnostic Test(s): While the clinical picture is highly suggestive, a definitive diagnosis requires a full thyroid panel. Relying on a single total T4 (TT4) value is insufficient, as many non-thyroidal illnesses and medications can falsely lower it (Euthyroid Sick Syndrome)

  • Definitive Thyroid Panel: A blood sample was submitted for a complete thyroid profile.

    • Protocol: The panel measured total T4, free T4 by equilibrium dialysis (the most accurate method), and canine thyroid-stimulating hormone (cTSH).

    • Results:

      • Total T4 (TT4): 0.5 µg/dL (Markedly Low) [Ref: 1.0 - 4.0 µg/dL]

      • Free T4 by Equilibrium Dialysis (fT4 by ED): 4 pmol/L (Low) [Ref: 8 - 40 pmol/L]

      • Canine Thyroid Stimulating Hormone (cTSH): 1.5 ng/mL (Markedly High) [Ref: 0.05 - 0.6 ng/mL]

    • Interpretation: This is the classic and definitive diagnostic signature for primary hypothyroidism. The low TT4 and fT4 levels confirm that the thyroid gland is failing to produce hormones. The high cTSH level confirms that the pituitary gland is functioning correctly and is trying to stimulate a thyroid gland that is no longer capable of responding.


Definitive Diagnosis: Primary Hypothyroidism. More information can be found at the Merck Veterinary Manual.


Treatment Plan: Treatment is straightforward and typically very rewarding, involving lifelong hormone supplementation.

  • Medication: Sadie was started on synthetic levothyroxine (L-thyroxine).

    • Dosing: The standard starting dose of 0.02 mg/kg was calculated, and she was prescribed 0.8 mg orally every 12 hours (BID). The owner was instructed to give the medication on a relatively empty stomach to ensure consistent absorption.

  • Expected Response: The owner was counseled on what to expect. An improvement in mental alertness and energy level should be noticeable within 1 to 3 weeks. The weight gain should stop, and she should begin to lose weight with appropriate diet and increased activity. The dermatologic signs are the slowest to resolve; hair regrowth may not be evident for 4 to 6 months.

  • Monitoring Protocol:

    • 4-Week Recheck: Sadie is scheduled to return in one month for a therapeutic monitoring check.

    • Post-Pill T4: On the morning of her recheck, the owner will give the morning dose of levothyroxine as usual. The blood sample to measure her total T4 level will be drawn 4 to 6 hours after the pill is administered.

    • Goal: The goal is for the post-pill TT4 level to be in the high end of the normal reference range or slightly above it (approximately 2.5-4.5 µg/dL). The dose will be adjusted based on this result and Sadie's clinical response. This monitoring will be repeated periodically throughout her life.

Case 33

Signalment and History: "Sadie," a 6-year-old, 38 kg (84 lb) female spayed Golden Retriever, is presented with the chief complaint that she is "acting old."

The owners report a slow, insidious decline in her energy and activity over the past year. Sadie, who was once an active family dog, is now lethargic, mentally dull, and prefers to sleep most of the day. She has gained nearly 10 lbs in the last year despite the owners being very careful with her diet and not giving her treats.

The owners also have significant dermatologic concerns. Sadie has developed a progressively thinning hair coat over her sides and back. The most dramatic change is the complete hair loss on her tail, which the owner describes as looking like a "rat's tail." Her skin seems flaky, and she has had two ear infections in the last six months, which is unusual for her. The owners state that the hair loss does not seem to bother her; she is not itchy. They are worried about her quality of life and what seems to be premature aging.

Physical Exam:

  • T: 100.8°F

  • P: 64 bpm (Bradycardia)

  • R: 20 bpm

  • BCS: 7/9 (Overweight)

  • Mentation: Quiet, calm, and slightly dull.

Sadie is quiet but cooperative for her exam. Her heart rate is slow and regular. The physical exam is most remarkable for its dermatologic findings:

  • Alopecia: There is a large area of bilaterally symmetrical, non-inflammatory, non-pruritic alopecia over the lateral trunk, lumbar region, and the bridge of her nose. The hair on her tail is almost completely absent, revealing hyperpigmented (darkened) skin underneath.

  • Coat Quality: The remaining hair coat is dry, brittle, and dull. The hair epilates easily with gentle traction.

  • Skin: The skin feels slightly thickened and cool to the touch. A mild, greasy seborrhea is present along her dorsum.

  • Facial Expression: A subtle "tragic" facial expression is noted, caused by mild puffiness of the skin above the eyes.

Initial Diagnostic Workup: A baseline database was established from a fasted blood sample.

  • Complete Blood Count (CBC): A mild, non-regenerative anemia is present (PCV: 34% [Ref: 37-55%]).

  • Serum Biochemistry Profile:

    • Cholesterol: Markedly elevated at 550 mg/dL [Ref: 110-320 mg/dL]

    • Triglycerides: Markedly elevated at 480 mg/dL [Ref: 50-100 mg/dL]

    • All other values, including liver and kidney enzymes, are within normal reference intervals.


What will be your tentative and differential diagnosis? 

What further diagnostic test(s) you will perform to confirm your diagnosis? 

What will be your treatment plan(s)?

Solution for Case 33 will be posted on Sept 26

Solution for Case 32

(Click here to see Case 32)

Tentative Diagnosis: The tentative diagnosis is Hyperadrenocorticism (HAC), or Cushing's Disease. The combination of the classic signalment, the insidious and progressive history of PU/PD, polyphagia, panting, and the hallmark physical exam findings (pot-belly, muscle atrophy, alopecia, thin skin) is strongly supported by the initial laboratory findings (especially the markedly elevated ALP and stress leukogram).


Further Diagnostic Test(s): The diagnostic plan involves a two-stage process: first, confirming the presence of hyperadrenocorticism, and second, differentiating between the pituitary-dependent (PDH) and adrenal-dependent (ADH) forms.

  1. Confirmation Test: The Low-Dose Dexamethasone Suppression (LDDS) Test was performed. This is considered the screening test of choice.

    • Protocol: A baseline cortisol sample was taken, a low dose of dexamethasone was injected IV, and blood samples were collected at 4 and 8 hours post-injection.

    • Results:

      • Basal Cortisol: 5.2 µg/dL

      • 4-hour Post-Dex Cortisol: 1.1 µg/dL (Suppression, as <1.4 µg/dL)

      • 8-hour Post-Dex Cortisol: 4.8 µg/dL (Failure to suppress, as >1.4 µg/dL)

    • Interpretation: The failure of cortisol to remain suppressed at 8 hours confirms the diagnosis of Hyperadrenocorticism.

  2. Differentiation Test: While the LDDS pattern (suppression at 4h, escape at 8h) is suggestive of PDH, an abdominal ultrasound was performed for more definitive localization.

    • Ultrasound Findings: Both adrenal glands were visualized and found to be symmetrically enlarged ("plump"), measuring 7.1 mm (left) and 6.9 mm (right) in width, with normal architecture. There was no evidence of a unilateral adrenal mass or atrophy of the contralateral gland.

    • Interpretation: This finding of bilateral adrenomegaly is consistent with constant stimulation from excess pituitary ACTH, confirming the pituitary-dependent form of the disease.


Definitive Diagnosis: Pituitary-Dependent Hyperadrenocorticism (PDH), or Cushing's Disease. For more, see the Merck Veterinary Manual.


Treatment Plan: The treatment goal is to manage the clinical signs and improve quality of life by reducing the body's cortisol production.

  • Primary Medication: Daisy was started on Trilostane (Vetoryl®). This medication is a competitive inhibitor of the 3β-hydroxysteroid dehydrogenase enzyme, effectively blocking the production of cortisol in the adrenal glands.

    • Dosing: A starting dose of 30 mg was prescribed to be given once daily with a meal to enhance absorption.

  • Concurrent Disease Management:

    • Hypertension: Daisy was started on Amlodipine to manage her systemic hypertension and reduce the risk of end-organ damage.

    • Proteinuria/UTI: A urine sample was submitted for culture and sensitivity to guide antibiotic therapy for her subclinical bacteriuria. Treatment for proteinuria with an ACE inhibitor (e.g., benazepril) was planned pending blood pressure control.

  • Monitoring Protocol: This is a critical component of safe and effective management.

    • 10-14 Day Recheck: Daisy is scheduled to return in 10 days for a re-evaluation. The owners will report on her thirst, appetite, and energy levels.

    • ACTH Stimulation Test: A precisely timed ACTH stimulation test will be performed 4-6 hours after she receives her morning dose of Trilostane. The goal is to see a post-stimulation cortisol level within the therapeutic range (typically 1.5–5.5 µg/dL), which indicates adequate control without over-suppression (which would risk an iatrogenic Addisonian crisis).

    • Long-Term: Once a stable dose is achieved, monitoring ACTH stimulation tests and biochemistry profiles will be performed at 1 month, 3 months, and then every 3-6 months thereafter for life.

Case 32

Signalment and History: "Daisy," a 9-year-old, 12 kg (26.4 lb) female spayed Miniature Poodle, is presented for evaluation of a constellation of clinical signs that have been progressing slowly over the past 18 months.

The owners provide a meticulous history. They first noticed an increase in Daisy's water consumption about a year and a half ago. This has now progressed to the point where she drinks constantly and has frequent urinary accidents in the house, despite having been perfectly house-trained her entire life. Her appetite, which was always good, is now described as "ravenous"; she begs for food relentlessly and scavenges for scraps.

Over the past year, her physical appearance has changed dramatically. She has developed a noticeably sagging, "pot-bellied" abdomen and pants heavily even while at rest in a cool room. Her once-thick coat of hair has thinned dramatically over her back and flanks, and the remaining hair is dry and brittle. Her skin seems thin, and she has developed what the owner calls "blackheads" on her belly. Despite her increased appetite, she seems weaker and more lethargic, hesitating to jump onto furniture.

Physical Exam:

  • T: 101.9°F

  • P: 120 bpm

  • R: Panting

  • BCS: 6/9

  • Blood Pressure (Doppler): 175 mmHg systolic [Ref: <160 mmHg]

Daisy is bright and alert but demonstrates generalized muscle weakness. The physical exam findings are striking and classic:

  • Abdomen: A tense, pendulous, pot-bellied abdomen is present, with hepatomegaly suspected on palpation.

  • Musculature: There is significant, symmetrical muscle wasting (atrophy) noted over the spine, ribs, and temporal bones of the head.

  • Dermatologic: A bilaterally symmetrical, non-pruritic alopecia (hair loss) covers the entire trunk. The underlying skin is thin, inelastic ("crepe paper skin"), and has poor wound healing noted from a recent scrape. The ventral abdomen shows prominent blood vessels, thin skin, and multiple large comedones.

  • Respiratory: The dog is panting constantly throughout the exam.

Initial Diagnostic Workup: A comprehensive baseline database was established.

  • Complete Blood Count (CBC): A classic stress leukogram is present, showing mature neutrophilia, lymphopenia, and eosinopenia.

  • Serum Biochemistry Profile:

    • Alkaline Phosphatase (ALP): Markedly elevated at 1,550 U/L [Ref: 23-212 U/L]

    • Alanine Aminotransferase (ALT): Mildly elevated at 190 U/L [Ref: 10-125 U/L]

    • Cholesterol: Elevated at 450 mg/dL [Ref: 110-320 mg/dL]

    • Glucose: Mildly elevated at 145 mg/dL [Ref: 75-125 mg/dL]

  • Urinalysis (Cystocentesis):

    • Urine Specific Gravity (USG): 1.014 (inappropriately dilute for a potentially dehydrated patient)

    • Dipstick: 2+ Proteinuria

    • Sediment: 3+ Bacteriuria with no white blood cells (pyuria) present, suggestive of a subclinical urinary tract infection.

  • Urine Protein:Creatinine (UPC) Ratio: 1.2 [Ref: <0.5], confirming significant renal protein loss.


What will be your tentative and differential diagnosis? 

What further diagnostic test(s) you will perform to confirm your diagnosis? 

What will be your treatment plan(s)?


Solution to Case 32 will be posed on Sept 19

Solution for Case 31

(Click here to see Case 31)

Tentative Diagnosis and Differentials: The tentative diagnosis is Diabetes Insipidus (DI). The clinical presentation of severe PU/PD in an otherwise healthy animal with persistently hyposthenuric urine is classic for this condition. The initial diagnostic workup successfully ruled out the most common differential diagnoses for severe PU/PD, including:

  • Diabetes Mellitus: Ruled out by normal blood glucose and negative urine glucose.

  • Chronic Kidney Disease: Ruled out by normal creatinine, BUN, and other chemistry values. Furthermore, the urine is hyposthenuric (actively diluted by the kidneys), not isosthenuric (passively unconcentrated) as would be expected with renal failure.

  • Hyperadrenocorticism (Cushing's Disease): Less likely given the lack of other clinical signs (e.g., pot belly, alopecia, skin changes) and the normal biochemistry profile.

  • Hypercalcemia & Liver Disease: Ruled out by the normal biochemistry profile.

The main remaining differential is Primary Polydipsia (Psychogenic Drinking), a behavioral condition. However, the presence of hypernatremia makes this less likely, as these patients tend to have normal to low sodium levels from overhydration. A definitive test is required for confirmation.


Further Diagnostic Test(s): The definitive test to confirm Diabetes Insipidus and to differentiate between its central and nephrogenic forms is the Modified Water Deprivation Test (MWDT), followed by an ADH response test.

  • Test Protocol and Results:

    1. Preparation: Kodiak was admitted to the hospital. His initial weight was recorded, the bladder was emptied, and all water was withdrawn. He was placed under constant observation in the ICU.

    2. Phase 1 (Deprivation): His body weight, urine specific gravity, and plasma osmolality were monitored hourly.

      • Hour 4: Kodiak lost 5% of his initial body weight, a clinical sign of significant dehydration. His plasma osmolality had increased, confirming dehydration.

      • Urine Concentration Check: Despite the clear evidence of dehydration, his USG remained profoundly dilute at 1.006.

      • Conclusion of Phase 1: A normal animal or one with psychogenic polydipsia would have concentrated its urine to a USG > 1.030 by this point. The failure to do so confirms a true concentrating defect and rules out psychogenic polydipsia. The diagnosis is now confirmed as Diabetes Insipidus. The next step is to determine the type.

    3. Phase 2 (ADH Response): An aqueous formulation of desmopressin acetate (DDAVP), an analog of ADH, was administered subcutaneously.

      • 1 Hour Post-DDAVP: USG increased to 1.018.

      • 2 Hours Post-DDAVP: USG increased dramatically to 1.035.

      • Conclusion of Phase 2: The dramatic and rapid increase in urine concentration after the administration of DDAVP demonstrates that the kidneys are perfectly capable of responding to ADH; they were simply not receiving the hormonal signal from the brain.


Definitive Diagnosis: Central Diabetes Insipidus (CDI). The underlying cause is likely idiopathic, as is common in many cases.


Treatment Plan: The treatment for CDI involves lifelong hormone replacement therapy.

  • Medication: The patient was prescribed Desmopressin Acetate (DDAVP) 0.1 mg/mL ophthalmic drops.

  • Administration and Dosing: The owner was instructed to instill one drop into the conjunctival sac of one eye every 12 hours. They were shown how to do this gently, without touching the bottle tip to the eye.

  • Monitoring and Titration: The owner will monitor the response at home by measuring Kodiak's daily water intake. The goal is to find the lowest dose and frequency (it may be possible to dose only once every 24 hours) that controls the clinical signs of PU/PD without causing over-concentration of urine or hyponatremia. The owner was instructed to keep a detailed log for the first two weeks.

  • Client Education: It was heavily emphasized that Kodiak must ALWAYS have free access to fresh water. If a dose is missed, he will temporarily become polyuric again, and restricting water at that time would be dangerous. The prognosis is excellent for a normal quality and duration of life with consistent medication and monitoring.

Case 31

Signalment and History: A 4-year-old, 25 kg (55 lb) male neutered Siberian Husky named "Kodiak" is presented for evaluation of severe and progressive polyuria and polydipsia (PU/PD) over the past six months.

The owner, a very attentive and concerned individual, provides a detailed history. The issue began subtly, with the dog needing to be let out to urinate once during the night, which was unusual for him. Over the past two months, the signs have become extreme. The owner reports filling a 2-gallon water bowl three to four times daily. The dog drinks incessantly and will seek water from any available source, including toilet bowls and puddles. The polyuria is equally dramatic; the dog produces large volumes of very clear urine and has started having accidents in the house if not let out at least every two hours, including multiple times overnight. The owner describes the urine as looking "exactly like water."

Critically, the owner reports an attempt to manage the issue last week by restricting water access for a few hours. Kodiak became extremely agitated, anxious, and frantic, digging at his empty water bowl. The owner quickly abandoned this attempt. Apart from the intense thirst and urination, the dog's appetite, energy level, and overall demeanor are reported as completely normal. He has no history of major medical issues and is current on all preventative care.

Physical Exam:

  • T: 101.7°F

  • P: 90 bpm

  • R: 20 bpm

  • MM: Tacky

  • CRT: < 2 sec

  • BCS: 5/9

Kodiak is a bright, alert, and responsive patient. He is well-muscled and in excellent body condition. The physical examination is remarkably unremarkable. No abnormalities are found on cardiac and pulmonary auscultation, abdominal palpation, or orthopedic/neurologic evaluation. The only subtle finding is that his mucous membranes are tacky, suggesting a borderline level of dehydration despite his constant water consumption. While in the exam room, he produced a very large volume of colorless urine on the floor.

Initial Diagnostic Workup: A comprehensive initial workup was performed to rule out common causes of PU/PD.

  • Complete Blood Count (CBC): All values within normal reference intervals.

  • Serum Biochemistry Profile: All values were within normal reference intervals with the exception of a mild hypernatremia (Sodium: 158 mEq/L [Ref: 142-152 mEq/L]).

  • Urinalysis (Free Catch):

    • Color: Clear/Colorless

    • pH: 7.0

    • Urine Specific Gravity (USG) by Refractometer: 1.004

    • Dipstick: Negative for glucose, ketones, protein, and blood.

    • Sediment Exam: Unremarkable.

Because of the critical importance of the USG, the measurement was repeated on two subsequent urine samples obtained over the next hour, yielding results of 1.002 and 1.006. The persistently and profoundly dilute urine (hyposthenuria) in the face of hypernatremia (which should be a powerful stimulus for the kidneys to conserve water) is a key finding.


What will be your tentative and differential diagnosis? 

What further diagnostic test(s) you will perform to confirm your diagnosis? 

What will be your treatment plan(s)?

Solution to Case 31 will be posted on Sept 12

Solution for Case 30

(Click here to see Case 30)

Diagnosis: The tentative diagnosis is severe insulin-resistant Diabetes Mellitus, with a very high suspicion for Feline Acromegaly (Hypersomatotropism) as the underlying cause. The combination of an older male cat with difficult-to-control diabetes requiring a massive insulin dose (> 1-2 U/kg), coupled with physical changes like weight gain, a broad head, and enlarged paws, is classic for this condition. 

DDx: Other causes of insulin resistance in cats must be considered. These include hyperadrenocorticism (Cushing's disease), chronic inflammation or infection (e.g., severe dental disease, urinary tract infection), pancreatitis, or problems with insulin handling and administration by the owner. However, the physical changes in this cat make acromegaly the top differential.

Diagnostic tests:

  • Screening Test: The single most useful screening test is measuring the serum concentration of Insulin-like Growth Factor 1 (IGF-1). GH from the pituitary tumor stimulates the liver to produce IGF-1, which will be markedly elevated.

    • Result: The cat's serum IGF-1 was 1,850 ng/mL [Reference: < 1,000 ng/mL]. This result is highly suggestive of acromegaly.

  • Definitive Diagnosis: Advanced imaging is required to identify the pituitary tumor. Contrast-enhanced CT or MRI of the head is the gold standard.

    • Result: A CT scan revealed a distinct, contrast-enhancing mass in the pituitary fossa.

  • Ancillary Diagnostics: An echocardiogram was recommended to investigate the heart murmur and screen for hypertrophic cardiomyopathy, a common secondary complication.

Definitive diagnosis: Acromegaly secondary to a functional pituitary adenoma, causing severe insulin resistance and Diabetes Mellitus.

Treatment: Treatment is focused on managing the diabetes and, if possible, addressing the pituitary tumor.

  1. Diabetes Management: The immediate goal is to control the clinical signs of diabetes. This cat will require continued high-dose insulin therapy, potentially increasing the glargine dose even further under careful monitoring. The goal is to keep the blood glucose below the renal threshold (~300 mg/dL) for most of the day to resolve the PU/PD, rather than achieving tight glycemic control.

  2. Tumor Treatment (Definitive Care):

    • The gold standard for treating the pituitary tumor is radiation therapy, specifically stereotactic radiosurgery (SRS). This can shrink the tumor, reduce GH secretion, and may even lead to remission of the diabetes.

    • Medical management with a somatostatin analog (e.g., pasireotide) can be attempted but is often cost-prohibitive and has variable efficacy.

  3. Monitoring: This cat requires lifelong monitoring. This includes regular glucose curves or fructosamine checks, monitoring for cardiac and renal complications, and watching for the development of neurologic signs (e.g., circling, altered mentation) that could arise from the expansion of the pituitary mass. For more information, see the Merck Veterinary Manual.

Case 30

An 11-year-old, 7 kg (15.4 lb) male neutered Domestic Shorthair cat is presented for a recheck of his Diabetes Mellitus, which was diagnosed 8 months prior. The owner is frustrated because the cat’s clinical signs of excessive thirst, urination, and appetite (PU/PD/PP) have not improved despite progressively increasing the insulin dose. The cat is currently receiving 12 units of glargine insulin twice daily. The owner also notes that the cat, despite being an uncontrolled diabetic, has actually gained weight and his head and paws seem larger.

Physical Exam:

  • T: 101.8°F

  • P: 190 bpm

  • R: 32 bpm

  • MM: pink/moist

  • CRT < 2 sec

The cat is a large-framed, well-muscled cat with a broad, blocky head and large paws. Mild prognathia inferior (protruding lower jaw) and widened spacing between the incisor teeth are noted. Cardiac auscultation reveals a new Grade III/VI systolic heart murmur. The abdomen is slightly pendulous, and the liver and kidneys feel subjectively large on palpation.

Biochemistry: (from a spot blood glucose check)

  • Glucose: 550 mg/dL [Ref: 75-125 mg/dL]

Fructosamine: (from 1 week prior)

  • Result: 610 µmol/L [Ref: < 350 µmol/L]


What will be your tentative and differential diagnosis? What further diagnostic test(s) you will perform to confirm your diagnosis? What will be your treatment plan(s)?


Solution to Case 30 (will be posted on Sept 5)

Solution for Case 29

(Click here to see Case 29

Diagnosis: The tentative diagnosis is Acute Congestive Glaucoma. The combination of a painful, red, cloudy eye with a fixed, dilated pupil and acute vision loss is highly suggestive of a rapid and severe increase in intraocular pressure. More information on this condition can be found at the Merck Veterinary Manual.

DDx: The main differential diagnoses for a painful red eye are severe anterior uveitis and a deep corneal abscess or melting ulcer. However, uveitis typically presents with a constricted (miotic) pupil, and an ulcer would be visible with a fluorescein stain.

Diagnostic tests: This is a true ophthalmic emergency, and diagnosis must be confirmed immediately.

  • Intraocular Pressure (IOP) measurement (Tonometry): This is the definitive diagnostic test. The pressure in both eyes was measured with a rebound tonometer (TonoVet/Tono-Pen).

    • Result OD (affected eye): 68 mmHg [Ref: 15-25 mmHg]

    • Result OS (normal eye): 22 mmHg

    • The extremely high IOP in the right eye confirms acute glaucoma.

  • Fluorescein stain: A stain was applied to the right eye to rule out a concurrent corneal ulcer before starting aggressive topical therapy. The test was negative.

Definitive diagnosis: Primary Acute Congestive Glaucoma. Given the breed (Cocker Spaniel) and the normal appearance of the other eye, a primary (inherited) cause is most likely.

Treatment: The goal is to rapidly reduce the IOP to save the optic nerve and preserve vision. Treatment must be aggressive and immediate. 🚑

  1. Emergency Medical Treatment:

    • An IV catheter was placed and a slow IV infusion of Mannitol (an osmotic diuretic) was started to rapidly draw fluid out of the eye.

    • A combination of topical medications was started in the right eye:

      • Latanoprost: A prostaglandin analog to increase uveoscleral outflow. One drop was given immediately. (Note: This is contraindicated if glaucoma is secondary to uveitis).

      • Dorzolamide-Timolol combination: A carbonic anhydrase inhibitor and a beta-blocker to decrease aqueous humor production. One drop was given, to be continued every 8 hours.

    • The IOP was rechecked every 30-60 minutes.

  2. Long-term and Prophylactic Treatment:

    • Once the IOP in the right eye was reduced to < 25 mmHg, the dog was started on a long-term topical medication plan (e.g., Dorzolamide-Timolol) to maintain normal pressure.

    • Prophylactic therapy (e.g., a single daily drop of a beta-blocker like Timolol) was started in the left ("good") eye, as primary glaucoma almost always becomes bilateral.

    • The owner was informed that medical therapy often fails over time and that the gold standard for long-term control is referral to a veterinary ophthalmologist for surgical options (e.g., laser cyclophotocoagulation or a gonioimplant).

Case 29

 A 6-year-old female spayed Cocker Spaniel is brought in for an emergency visit. The owner reports that the dog woke up this morning with a very red, cloudy right eye (OD). The dog is keeping the eye shut, is refusing to eat, and seems lethargic and painful. The owner does not know of any trauma. The left eye (OS) appears normal.

Physical Exam:

  • T: 102.6°F

  • P: 130 bpm

  • R: Panting

  • MM: pink/moist

  • CRT <2 sec

The dog is visibly depressed and in pain, resenting any handling of her head. The ophthalmic exam of the right eye (OD) reveals severe blepharospasm. When the eyelids are opened, there is marked episcleral injection (intense redness of the "white" of the eye) and diffuse, steamy-looking corneal edema. The pupil is mydriatic (dilated) and unresponsive to a bright light source. A menace response is absent in the right eye. The left eye (OS) appears normal on gross examination.

CBC and Biochemistry:

  • All values are within the reference range.

Urinalysis:

  • Not performed at presentation.


What will be your tentative and differential diagnosis? What further diagnostic test(s) you will perform to confirm your diagnosis? What will be your treatment plan(s)?

Solution to Case 29 will be posted on Aug 29

Solution for Case 28

(Click here to See Case 28

Diagnosis: Tentative diagnosis is unilateral anterior uveitis based on the classic ophthalmic exam findings of a painful, red, cloudy eye with miosis and aqueous flare. The systemic signs (fever, lethargy) and lab abnormalities (thrombocytopenia, hyperglobulinemia) strongly suggest an underlying systemic, likely infectious, cause.

DDx:

  • For the red eye: The primary differentials include glaucoma and a deep corneal ulcer with reflex uveitis.

  • For the underlying cause of uveitis: Given the signalment and history (hunting dog, rural area) and the finding of thrombocytopenia, tick-borne infectious diseases (e.g., Ehrlichia canis, Rocky Mountain Spotted Fever) are high on the list. Other considerations include systemic fungal infections (e.g., Blastomycosis), protozoal infections, neoplasia (e.g., lymphoma), and immune-mediated disease.

Diagnostic tests:

  • Ophthalmic diagnostics:

    • Intraocular Pressure (IOP) measurement (Tonometry): To differentiate from glaucoma. Uveitis typically causes a low IOP. Result in this case: OS = 8 mmHg, OD = 17 mmHg [Ref: 15-25 mmHg]. This low pressure in the affected eye supports the diagnosis of uveitis.

    • Fluorescein stain: To rule out a corneal ulcer before starting topical steroids. The stain was negative in this case.

  • Systemic diagnostics:

    • Infectious Disease Panel: A blood sample was submitted for a 4Dx Plus SNAP test and tick-borne disease PCR panel. The 4Dx test was positive for Ehrlichia canis antigen.

    • Thoracic Radiographs: Three-view chest x-rays were performed to screen for fungal disease or metastatic neoplasia, which were unremarkable.

Definitive diagnosis: Anterior uveitis secondary to systemic Ehrlichia canis infection.

Treatment: The treatment plan is twofold: control the ocular inflammation to preserve vision and treat the underlying systemic infection.

  1. Ocular Treatment:

    • Topical anti-inflammatory: Prednisolone acetate 1% ophthalmic suspension, 1 drop in the left eye every 6 hours to control the inflammation.

    • Topical mydriatic/cycloplegic: Atropine 1% ophthalmic ointment, a small strip applied to the left eye every 12 hours. This dilates the pupil to relieve the pain from ciliary muscle spasms and to prevent the iris from scarring down to the lens (posterior synechiae).

  2. Systemic Treatment:

    • Antibiotic: The dog was started on Doxycycline at 10 mg/kg orally once daily for 28 days to treat the Ehrlichia infection.

    • Systemic anti-inflammatory: A short, anti-inflammatory course of a systemic NSAID (e.g., Carprofen) was considered for the fever and discomfort but held in reserve to monitor initial response.

Monitoring: The patient will be re-evaluated in 3-5 days to check the intraocular pressure and assess the response of the uveitis to topical therapy. The atropine frequency will be reduced as the pupil remains dilated, and the prednisolone will be tapered slowly over several weeks based on clinical response. The dog's platelet count and clinical signs will be monitored for response to the doxycycline.

Case 28

 A 5-year-old intact male German Shorthaired Pointer is presented with a 3-day history of squinting his left eye (OS). The owner reports the eye appears red and hazy, and the dog is less active than usual with a decreased appetite. He is an active hunting dog, is up to date on vaccinations, and spends a lot of time in a wooded, rural area. The owner has not noticed any trauma to the eye.

Physical Exam:

  • T: 103.4°F

  • P: 90 bpm

  • R: 24 bpm

  • MM: pink/moist

  • CRT <2 sec

The general physical exam reveals mild lethargy and a low-grade fever. On ophthalmic exam, the left eye (OS) shows marked blepharospasm, moderate conjunctival and episcleral hyperemia (a "red eye"), and diffuse corneal edema (a "hazy" or "cloudy" appearance). The pupil is constricted (miosis) and responds poorly to light. Using a transilluminator in a dark room, a faint "flare" is visible in the anterior chamber, indicating increased protein. The right eye (OD) appears normal.

CBC and Biochemistry:

  • CBC: Mild thrombocytopenia (Platelets: 120 K/uL [Ref: 175-500 K/uL])

  • Biochemistry: Mild hyperglobulinemia (Globulins: 4.5 g/dL [Ref: 2.5-4.5 g/dL]). All other values are within reference range.

Urinalysis:

  • All values within reference range.


What will be your tentative and differential diagnosis? What further diagnostic test(s) you will perform to confirm your diagnosis? What will be your treatment plan(s)?


Solution for Case 28 will be posted on Aug 22

Solution for Case 27

 Solution for Case 27 

(Click here to see Case 27)

Diagnosis: Tentative diagnosis is Diabetes Mellitus based on the hallmark clinical signs of polyuria, polydipsia, polyphagia, and weight loss, in conjunction with significant hyperglycemia and glucosuria.

DDx: The primary differential diagnoses for significant PU/PD in a dog include Hyperadrenocorticism (Cushing's Disease) and Chronic Kidney Disease (CKD). However, the profound hyperglycemia and glucosuria make Diabetes Mellitus the leading diagnosis.

Diagnostic tests:

  • The combination of persistent fasting hyperglycemia (blood glucose > 250 mg/dL) and glucosuria is diagnostic for Diabetes Mellitus in dogs. Stress hyperglycemia in dogs rarely exceeds 200 mg/dL, so the value of 485 mg/dL is definitive.

  • A fructosamine level could be measured to confirm sustained hyperglycemia over the previous 2-3 weeks, but it is not strictly necessary for diagnosis in this case given the classic signs and degree of hyperglycemia.

  • The presence of trace to small ketones in the urine indicates the body is breaking down fat for energy and warns of the potential to progress to Diabetic Ketoacidosis (DKA), a medical emergency. Since this patient is still eating and appears bright, she is classified as having uncomplicated diabetes.

Definitive diagnosis: Diabetes Mellitus with secondary diabetic cataracts.

Treatment: The goals of treatment are to eliminate the clinical signs, prevent complications like DKA and hypoglycemia, and provide a good quality of life.

  • Insulin Therapy: This patient was started on an intermediate-acting insulin. A common starting choice is a porcine lente insulin (Vetsulin®) or NPH insulin (Humulin-N®, Novolin-N®) at a dose of 0.25 - 0.5 Units/kg every 12 hours. The injections are given subcutaneously immediately following a meal.

  • Dietary Management: The dog will be transitioned to a prescription therapeutic diet formulated for diabetic dogs, which is typically high in fiber and complex carbohydrates. The owner was instructed to feed two equal-sized meals every 12 hours, just prior to each insulin injection. No other treats or food should be given to ensure consistent glucose absorption.

  • Client Education & Monitoring: This is a critical component of management. The owner was taught how to handle and administer insulin and educated on the signs of hypoglycemia (weakness, lethargy, stumbling, seizures). The plan is to have the dog return in 7-10 days to perform a blood glucose curve, where blood glucose is measured every 2 hours for 12 hours to assess the insulin's effectiveness and duration. The dose will be adjusted based on the curve results and the resolution of clinical signs.

  • Cataracts: The owner was informed that the cataracts are a direct and common result of diabetes in dogs and are unlikely to resolve. Once the dog's diabetes is well-regulated, she can be referred to a veterinary ophthalmologist to discuss surgical cataract removal to restore vision.

Case 27

 Case 27

A 7-year-old female spayed Beagle mix is presented for a 3-week history of drinking and urinating excessively (polyuria/polydipsia). The owner reports the dog has an excellent appetite but has lost a noticeable amount of weight. Over the last few days, the owner thinks the dog’s eyes have developed a "cloudy" appearance and she has been bumping into furniture. The dog is up to date on vaccinations and preventatives.

Physical Exam:

  • T: 101.9°F

  • P: 110 bpm

  • R: 28 bpm

  • MM: pink/moist

  • CRT <2 sec

The dog is bright and alert but has a slightly thin body condition (BCS 4/9). The remainder of the physical exam is unremarkable except for the ocular exam, which reveals bilateral, symmetrical, dense opacities within the lenses consistent with mature cataracts.

CBC and Biochemistry:

  • CBC: All values within reference range.

  • Biochemistry:

    • Glucose: 485 mg/dL [Ref: 75-125 mg/dL]

    • Alanine Aminotransferase (ALT): 180 U/L [Ref: 10-125 U/L]

    • Alkaline Phosphatase (ALP): 350 U/L [Ref: 23-212 U/L]

    • All other values are within reference range.

Urinalysis: (performed on a free-catch sample)

  • Color: Clear

  • pH: 6.0

  • SG (refractometer): 1.012 [Ref: >1.025]

  • Protein (dipstick): Trace

  • Glucose (dipstick): 4+ (>1000 mg/dL) [Ref: Negative]

  • Ketones (dipstick): 1+ (Small) [Ref: Negative]

  • Sediment exam: Unremarkable


What will be your tentative and differential diagnosis? What further diagnostic test(s) you will perform to confirm your diagnosis? What will be your treatment plan(s)?

Solution for Case 27 

Solution for Case 26

 

Solution for Case 26

Diagnosis: Tentative diagnosis is feline hyperthyroidism based on the classic signalment (older cat) and clinical signs (weight loss, polyphagia, PU/PD, tachycardia, palpable thyroid nodule).

DDx: The main differential diagnoses for a cat with weight loss and PU/PD include Chronic Kidney Disease (CKD) and Diabetes Mellitus. Gastrointestinal disease (e.g., Inflammatory Bowel Disease, GI lymphoma) could also cause weight loss, but less commonly causes significant PU/PD.

Diagnostic tests:

  • Total Thyroxine (T4) Concentration: A single blood sample was submitted for a total T4 measurement.

    • Result: 9.8 µg/dL [Reference Range: 0.8–4.0 µg/dL]

  • This significantly elevated T4 level is diagnostic for hyperthyroidism.

  • Blood Pressure Measurement: Given the tachycardia and heart murmur, blood pressure was measured using a Doppler.

    • Result: 175 mmHg systolic [Reference: <160 mmHg]

    • This result confirms systemic hypertension, a common complication of hyperthyroidism.

Definitive diagnosis: Feline Hyperthyroidism with secondary systemic hypertension.

Treatment: There are four main treatment options for feline hyperthyroidism: medical management, radioactive iodine therapy, therapeutic diet, and surgical thyroidectomy.

  • This patient was started on medical management to stabilize her condition. She was prescribed Methimazole 2.5 mg orally twice daily. Methimazole works by blocking the synthesis of thyroid hormones in the thyroid gland. The owner was warned to watch for potential side effects, including facial excoriations, vomiting, or lethargy.

  • For the systemic hypertension, the cat was also started on Amlodipine 0.625 mg orally once daily.

  • Monitoring Plan: The patient will be re-evaluated in 2 weeks. The recheck appointment will include a physical exam, blood pressure measurement, and a blood draw to check her Total T4, creatinine, and BUN. The creatinine and BUN are monitored closely because treating hyperthyroidism can "unmask" underlying kidney disease by decreasing the glomerular filtration rate (GFR). Once a stable dose of methimazole is achieved (T4 in the low-normal range), she will be monitored every 3-6 months. The owner was also educated on the benefits of radioactive iodine (I-131) therapy as a potential cure once the cat is stable.

Case 26

 Case 26

An 11-year-old spayed female Domestic Shorthair cat was presented to the clinic with a 2-month history of progressive weight loss despite a ravenous appetite (polyphagia). The owner also reports increased thirst and urination (polyuria/polydipsia) and occasional vomiting for the past few weeks. The cat has become more vocal and restless, especially at night. She is an indoor-only cat and is current on all preventative care.

Physical Exam:

  • T: 102.9°F

  • P: 230 bpm

  • R: 40 bpm

  • MM: pink/moist

  • CRT <2 sec

The cat is thin with a body condition score of 3/9 and has palpable muscle wasting over the spine and hips. The hair coat is unkempt and mildly greasy. Cardiac auscultation reveals a tachycardia with a Grade II/VI systolic heart murmur. Careful palpation of the ventral neck reveals a small, firm, movable nodule on the right side, consistent with a "thyroid slip".

CBC and Biochemistry:

  • CBC: Mild erythrocytosis (PCV 48% [Ref: 29-45%])

  • Biochemistry: Alanine Aminotransferase (ALT): 155 U/L [Ref: 12-130 U/L]. All other values are within reference range.

Urinalysis:

  • Color: Pale yellow

  • pH: 7.0

  • SG (refractometer): 1.020 [Ref: >1.035]

  • Protein (dipstick): Trace

  • Blood (Dipstick): Negative

  • Sediment exam: Unremarkable


x

What will be your tentative and differential diagnosis? What further diagnostic test(s) you will perform to confirm your diagnosis? What will be your treatment plan(s)?

Solution for this case