Transcript Interesting case - ::: อายุรศาสตร์

Interesting case
17/05/07
Naree Panamonta, MD.
ผูป้ ่ วยหญิงอายุ 20 ปี อาชีพนักศึกษาปวส.
CC: ปวดศีรษะตามัว 2 เดือนก่อนมารพ.
PI: 6 เดือนPTA ปวดศีรษะเป็ นๆหายๆ กินยา
paracetamol ทุเลาลง ไม่ได้ไปพบแพทย์
2 เดือนPTA ปวดศีรษะตื้อๆที่ขมับสองข้าง มีคลื่นไส้ แต่
ไม่อาเจียนเป็ นเกือบตลอดเวลา เวลาปวดมาก pain score
10/10 ต้องกินยา paracetamol 2 tab/ครั้ง
ประมาณ 3-4 tab/วัน อาการ progress มากขึ้นเรื่ อยๆ
ไม่มีผนื่ ไม่มีผมร่ วงหรื อปวดข้อ ไม่ได้ไปพบแพทย์
1 เดือน PTA เริ่ มมีตามัวสองข้าง เห็นจุดสี ดากลางตา คลื่นไส้
มากขึ้น ไม่อาเจียน ไม่มีแขนขาอ่อนแรง
3 wk. PTA ตามัวมองเห็นไม่ชดั มากขึ้นทั้งสองข้าง ปวดศีรษะ
เท่าๆเดิม ไม่มีข้ ีร้อน/ใจสัน่ /มือสัน่ ปัสสาวะออกเท่าเดิม มีนน.
ลด 10 kg. ไปรพช.2 ครั้งบอกเป็ น neuroretinitis
both eyes refer มารพ.ศรี นคริ นทร์ ไม่ได้ check
BP, VDRL-neg
5 day PTA มาตรวจที่ OPD eye ตรวจพบ
eye ground- Disc swelling, dot
hemorrhage, cotton wool spot, flame
shape hemorrhage, mild vvs.
tortuosity both eyes, macula edema
ไม่ได้วดั BP เจาะ lab ไว้แล้วนัด F/U
2 day PTA หอบเหนื่อยมากขึ้น หายใจไม่อิ่มนอนราบไม่
สะดวก ปัสสาวะยังออกดี
วันมารพ. มาตรวจ OPD eye ตามนัด วัดBPได้ 220/140
mmHg ส่ งมา OPD 8
Physical exam
GA- A young female, looked pale, fatigue,
cachexia.
V/S- BP 214/150 mmHg, PR 124/min, RR 22
/min
BP 4 extremities: 215/155
205/143
255/148
220/141
HEENT- Marked pale, no jaundice, CLN-ve
No engorged neck vein.
Thyroid gland not enlarged.
Heart- Active precordium. LV heavingpositive. PMI at 6th ICS, 2 cm. lateral
to MCL. Tachycardia, regular HR. No
murmur.
Lungs- Crepitation both basal lungs.
Abdomen- Soft, liver and spleen not
palpable. No renal bruit.
Ext.- No edema. Equal pulses, no
bounding pulse. No tremor, no moist
skin.
Neuro- E4M6V5. Pupils 3 mm RTL, BE.
Eye ground- Blur disc with cotton wool
spot with flame shape
hemorrhage.Copper wire changes of vvs.
CN intact all.
Motor gr.V all. DTR 2+.
BBK- plantar flexion both.
Clonus- neg.
Problems
1. Hypertensive emergency ( malignant HT)
with Target organ damaged
- CNS: hypertensive retinopathy +
encephalopathy
- Acute pulmonary edema
2. Suspected secondary hypertension
CBC:
Hb 11.3, Hct 33, WBC 11,800 ( N 68,L 19.1, Mo
10.1, Eo 1.4) Plt 136,000, MCV 82
UA:
Sp. 1.010, pH 7.0, Alb 4+, Glu –ve, RBC 5-10,
WBC 10-20, Hyaline cast 10-20,
Granular cast 10-20, Epi 1-2
BUN 14.8, Cr 1.8
Elyte: Na 137, K 3.3, HCO3 25.6, Cl 106
Ca 8.6, PO4 4.1, Mg 2.2
LFT- Chol 201, Alb 3.7, Glob 3.6, TB 1.9, DB 0.2,
ALT 16, AST 40, ALP 74
Chest X-ray:
LV hypertrophy, cephalization of
pulmonary vein, Kerley’s B line.
EKGSinus tachycardia, LVH by voltage, No
LV strain pattern
Film KUB- Not seen stone
Urine Elyte- Na 10, K 41.1, Cl 22
Urine 24 hr- Cr 0.6, Prot 2,409 mg/vol,
Vol= 760 ml. GFR= 23
Serum osmole 287, Urine osm. 573
TTKG = 6.2
ANA – negative
Anti- HIV: Non reactive
TFT- FT3 4.13 (2.3- 6.9 pg/ml)
FT4 2.58 (0.78- 2.11 ng/dL)
TSH 5.21 (0.2- 3.2 mIU/ml)
Ultrasound KUB
Increase parenchymal echogenicity with
loss of corticomedullary differentiation.
Kidney size: Rt.9.15 cm., Lt. 8.69 cm.
Cortical thickness: Rt. 0.98 cm., Lt. 1.42
cm.
No hydronephrosis.
Problem lists
1. Hypertensive emergency ( malignant HT)
with Target organ damaged
- CNS: hypertensive retinopathy
- Acute pulmonary edema
- R/O Hypertensive nephropathy
2. Secondary hypertension
3. Hypokalemic metabolic alkalosis
Differential Dx of 2ry HT cause
1. Renal parenchymatous disease
- Chronic glomerulonephritis
: Chronic- Hx of prolong symptoms,
eye ground changes
: Impaired renal function, nephritic
ranged proteinuria, active urinary
sediments
2. Hyperaldosteronism
: Hypokalemia, metabolic alkalosis
Differential Dx of 2ry HT cause
3. Renovascular hypertension
4. Pheochromocytoma
5. Other endocrine HT: hyperthyroidism
(TFT- WNL)
Management (this case)
• Diltiazem IV drip
• NTG IV drip
• Add oral hypertensive medications:
- Nifecard retard, Prazocin,
Hydralazine, Methyldopa, Metoprolol
• Collect urine VMA 24 hr.
• Kidney biopsy
• CT adrenal gland
Kidney biopsy patho (H&E stain):
Arteriolar medial thickening.
Increased mesangial matrix.
Tubulointerstitial change.
Imp: Malignant hypertensive
nephrosclerosis
Urine 24 hr. VMA
27/04/50
10.1 ug/mg Cr
28/04/50
11 ug/mg Cr
29/04/50
4.4 ug/mg Cr
(1.5- 7.0)
CT adrenal gland
- Non enhancing posterior Lt. pararenal mass
contains fat density.
- Normal both adrenal glands.
- Small liver nodule at segment 7 about 1 cm. in
diameter.
Imp: Lt. posterior pararenal mass contains fat
density DDx retroperitoneal mass.
Malignant Hypertension
due to Secondary HT
Effects of HT (TOD)
1. Heart
- Concentric LV hypertrophy
- Myocardial ischemia/ infarction
- Congestive heart failure
2. Neurologic
- Retinal and CNS dysfunction
- Dizziness, light-headedness, vertigo, tinnitus,
syncope
- Cerebral infarction/ hemorrhage
- Hypertensive encephalopathy: severe HT,
impaired consciousness, increased ICP, retinopathy
with papilledema, seizure
Effects of HT (TOD)
3. Kidney
- Atherosclerosis of afferent and efferent
arteriole, glomerular capillary tufts
- Decrease GFR, tubular dysfunction
- Glomerular disease as a cause:
proteinuria, microscopic hematuria
Hypertensive emergency
• Diastolic BP > 120 mmHg
• Severe acute target organ damage
- Hypertensive encephalopathy: severe
headache, vomiting, visual disturbances,
transient paralysis, convulsion, stupor,
coma
- Cardiac decompensation
- Rapidly declining renal function
Hypertensive emergency
• Vascular lesion
- Fibrinoid necrosis of walls of small
arteries arterioles
- Cerebral arteries dilate
excessive
cerebral blood flow
• Microangiopathic hemolytic anemia ( 2ry
to deteriorate renal function)
Hypertensive emergency:
Management
• Rapid acting IV antihypertensive agent
- Labetalol, Fenoldopam, Nitroprusside,
Nimodipine
- Decrease DBP 10-15% in < 1 hr.( not to
level < 95 mmHg)
• IV nitrate + furosemide in acute pulmonary
edema
• Correction underlying disease
Hypertensive Retinopathy
• In 1939, Keith et. al. ----predictive of
death in HT patients
• Classification system: Keith-WagenerBarker classification – categorized
into 4 groups of increasing severity
• Signs of hypertensive retinopathy
regress with control of BP
Hypertensive nephrosclerosis
• Present with HT& its complications (eg, heart failure,
stroke), and/or symptoms of uremia.
• Features suggesting HN :
- Black race
- Hypertensive retinal changes
- Left ventricular hypertrophy
- Long-standing (usually >10 y) or very severe
hypertension
- Proteinuria less than 0.5 g/d
- Hypertension diagnosed prior to onset of proteinuria
- Hypertension preceding renal dysfunction
- No evidence of another renal disease
- Biopsy findings compatible with the diagnosis
Hypertensive nephrosclerosis
 - 30% present with declined GFR at
presentation
 - Some patients with biopsy-proven
HN have 24-hour urinary protein
increase to the nephrotic range when
secondary changes of FSGS present
Glomeruli obsolescence,
interstitial fibrosis, arterial
intimal fibroplasia,
arteriolar hyalinization in
arterioles
Wrinkling of the
glomerular tuft and
thickening of the
Bowman capsule
Glomerular
hyalinosis and the
development of
secondary tubular
atrophy and
interstitial fibrosis
Hypertensive nephrosclerosis
• Antihypertensive therapy and ACE
inhibitor
- Nephrosclerosis is part of generalized
vascular disease
- Patients with cardiovascular disease
and impaired renal function benefit more
than those with normal kidney function
- BP control magnify long-term
cardiovascular risk
Essential vs. Secondary HT
4% 1% 1%
Essential HT
Renal
Renovascular
Endocrine & Misc.
94%
2ry HT is suspicion
1. Age <35 or > 55
2. Therapeutic failure with initial drug
program(3-drug rx.)
3. BP >180/110 mmHg
4. Sudden↑ BP in well-controlled HTN
2ry HT is suspicion
5. Signs & symptoms of specific disease
- HA/palpitation/pallor/sweats
- Renal bruits
- SBP in legs < 20 mm SBP in arms
- Cushing's physical stigmata
6. Abnormal lab
- K+ <3.5
- Elevated creatinine
- Elevated calcium
- Abnormal UA
Causes of 2ry HT
• Renal HT
Renal parenchymal
Renovascular
• Endocrine HT
1ry aldosteronism
renin producing tumor
Cushing’s syndrome
Pheochromocytoma
Hyperthyroidism
Hypercalcemia
Acromegaly
Causes of 2ry HT
• Vascular cause - Coarctation of aorta
• Obstructive sleep apnea
• Medications: OCPs, Cocaine, EtOH
Renal Parenchymal Disease
• Single largest cause of secondary
hypertension
• Most are irreversible.
• Acute renal failure
- Acute glomerulonephritis (especially
post-infectious, crescentic, or focal
segmental changes)
- Vasculitis (esp. SLE, scleroderma, or
polyarteritis
- Acute obstruction
Renal Parenchymal Disease
• Chronic renal failure: nephron loss>80%
- Vasculitis
- Glomerular disease (especially
diabetic nephropathy and crescentic or
focal segmental glomerulitis)
- Polycystic renal disease
Chronic glomerulonephritis
1. Rapidly progressive glomerulonephritis (RPGN)
or crescentic glomerulonephritis
- 90% progress to ESRD within weeks or
months.
2. Focal segmental glomerulosclerosis (FSGS)
- 80% progress to ESRD in 10 years
- Collapsing variant
: Malignant FSGS, have more rapid
progression
: Idiopathic or related to HIV infection.
3. Membranous nephropathy
- 20-30% progress to chronic renal failure (CRF)
and ESRD in 10 years.
Chronic glomerulonephritis
4. Membranoproliferative glomerulonephritis
(MPGN)
- 40% progress to CRF and ESRD in 10 years.
5. IgA nephropathy
- 10% progress to CRF and ESRD in 10 years.
6. Poststreptococcal glomerulonephritis
- 1-2% progress to CRF and ESRD.
- Older children or adults with crescentic
glomerulonephritis are at greatest risk
Chronic glomerulonephritis
• Hemodialysis + antihypertensive may
increase survival in malignant
hypertension associated with severely
damaged renal function
• Difficult to distinguish
- HT is a consequence of nephritis or
consequence of renal failure
Renovascular HT
• Fibromuscular dysplasia of renal arteries
- About 25% of all renovascular HT
- Young females
• Atherosclerotic disease
- Nearly 70% of the total
- Generally arise bilaterally
• Arteriography- gold standard
: Critical stenoses of ≥80%
Renovascular HT
• ACE-inhibitor produces a fall GFR on the
affected side.
• Positive scan correlates with successful
angioplasty or surgical intervention in
≥ 90% (less definitive in the presence of
renal dysfunction)
Hyperaldosteronism
• Primary hyperaldosteronism
- Adenoma, carcinoma, or bilateral hyperplasia
- Enzymatic deficiencies (11-OH-hydroxylase
deficiency, 17-OH-hydroxylase deficiency, and
11-OH-dehydrogenase deficiency syndromes)
- Chronic licorice ingestion
• Non-specific weakness, fatigue, polyuria, or
cramps (reflecting hypokalemia)
Hyperaldosteronism
• Best screening test : 24-hour urinary
collection for aldosterone
• Simpler screening test : Plasma aldosterone
to plasma renin activity (PRA) ratio
• PA/PRA ratio >30 and a PA >20 ng/ml
(withdrawn from antihypertensive
medications for ≥two weeks)
Pheochromocytoma
• Nearly 80% of the tumors limited to
adrenal glands
- Usually unilaterally
- Bilateral or multiple in
neurofibromatosis, Von Hippel-Lindau
disease, or MEN type 2a or 2b
• 10-20% intra-abdominal sites, <5% from
intrathoracic sites
Pheochromocytoma
• Classic triad : episodic headache,
palpitations with or without tachycardia,
and inappropriate perspiration
• Definitive diagnosis and full localization
requires both
: Biochemical tests for catecholamines
: Scanning potential sites by CT or MRI
Medications
- Vasoconstrictors : phenylephrine, pseudoephedrine,
phenylpropanolamine, β-agonist bronchodilators,
ephedrine, cocaine, stimulant abuse, anti-adrenergic
agent withdrawal, and MAOI cotreatment with
tyramine-containing foods
Volume expanders (glucocorticoids, estrogens at
high doses, NSAIDS
Poorly specified mechanisms such as cyclosporine,
tacrolimus, or erythropoietin
Miscellaneous other agents like psychotropic
drugs that interfere with sympatholytic
antihypertensive agents
Thank you for your attention