SAPS III

AKIKI有用一個scoring system: SAPS III 

查了一下，似乎是比較新的（2003以後出來的）

based on SAPS II的基礎去做出的一個指標

http://www.saps3.org/news/ 

這是它的官方網站

似乎是蠻複雜的參數

有時間應該要好好看它怎麼評估病人

下面這個是1994年SAPS II

2004年發表的SAPS III

HAART failure definition

Washington maunual, 35/e, chap. 16

HAART failure definition:

1. less than a log (10-fold) reduction of the viral load 4-6 weeks after starting a new ART
2. failure to reach an undetectable viral load after 6 months of Tx
3. detection of the virus after initial complete suppression of viral load => possible resistant
4. persistent decline of CD4 cell count or clinical deterioration

4-6 weeks after initiation of ART => viral load and CD4 count

Q3-6M regular follow under stable medication control

PI and cobicistat both inhibit andinduce the P450 system => macrolides, antifungals, rifamycins, anticonvulsants; antihistamines, antiarrhthmic (flecainide, encainide, quinidine), fentanyl, meperidine, midazolam, warfarin, statin (pravastatin is the safest), oral contraceptives

2016 NEJM--Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit

2016 NEJM--Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit

Purpose:

The best timing for RRT in ICU patients with AKI is unknown.

Despite progress in RRT management, mortality remains high and the timing of its initiation remains open to debate when no metabolic disorder (severe hyperkalemia or metabolic acidosis) or major fluid overload threaten short term prognosis. Such abnormalities mandate RRT and are non-inclusion criteria of our study.

=> whether duration of oliguria/anuria and /or value of serum urea/creatinine are an adequate indications for RRT is unknown.

Hypothesis:

“Delayed” strategy would prove beneficial to the patients and would translate into increased survival.

=> This study is designed to prove superiority (and not noninferiority) of this strategy over the “early” one.

Objective:

Main objective to compare two strategies of RRT initiation in terms of overall survival in ICU patients (mechanically ventilated and/or receiving catecholamine infusion) with severe AKI defined as RIFLE F classification.

Early strategy

Delayed strategy

RRT immediately when a RIFLE F status is documented

RRT in patient with RIFLE F only in case of occurrence of one or more of the follow events (“Alert Criteria”): oliguria or anuria for more than 72 hours after randomization SUN > 40mmol/L (112 g/dL) Serum K > 6 mmol/L, Serum K > 5.5 mmol/L that persists despite well-conducted medical treatment with at least NoHCO3 and/or glucose/insulin infusion ABG pH < 7.15: pure metabolic acidosis, (PaCO2<35) ABG pH < 7.15: mixed acidosis w/ PaCO2>50 w/o possibility of lowering PaCO2 value Acute overload pulmonary edema => severe hypoxemia requiring O2 flow > 5L/min in spontaenously breathing patients despite diuretic use Acute overload pulmonary edema in patient ventilated (w/ invasive or noninvasive) with > FiO2 > 50%

Design: Prospective, multicenter, randomized, open-label trial comparing two RRT initiation strategies in terms of overall survival

Primary endpoint:

Overall survival, measured from the date of randomization to the date of death, regardless of the cause. Minimun duration: 60-day follow-up

Secondary endopoints:

1. survival rate at D28
2. % of patients requireing who did not require RRT in the delayed strategy
3. timie unitl cessation of RRT therapy
4. Rate of adverse events potentially related to the AKI or to RRT (eg; RRT catheter related complicates, hemorrhage due to anticoagulation required for RRT etc…)
5. rate of nosocomial infections
6. # of vetilator free days of RRT free days and of vasopressors free days
7. length of stay in ICU and hospital
8. rate of limitations of treatment for futiligy
9. total cost of connsumables (including RRT catheters and lines among others) related to RRT between D1 and D28

Inclusion criteria:

1. ICU patients
2. Age > = 18 years
3. AKI compatible with the dx of ATN defined by clinical ischemic or toxi insult
4. AKI, with RIFLE F classification: (one of the following 3)
1. Creatinine > 354 mmol/L (4mg/dL) or > 3 times the baseline
2. anuria for more than 12 hours
3. oliguria defined as U/O < 0.3ml/kg/hr or 500ml/d for more than 24 hours
5. Mechanical ventilation and/or catecholamines infusion (noradrenaline or/and adrenaline)

Non-inclusion criteria:

1. CKD (defined as creatinine clearance < 30ml/min)
2. Patients already enrolled in the study
3. Inclusion criteria #4 present for more than 5 hours
4. AKI due to
1. urinary tract obstruction
2. renal vessels obstruciton
3. tumor lysis syndrome
4. thrombotic microangiopathy
5. acute GN
5. Intoxication with a dialyzable product
6. Child-Pugh class C liver cirrhosis
7. Renal transplant
8. Cardiac arrest without awakening at time of potential inclusion
9. Moribund state
10. decision to limit treatment
11. RRT already started for the current episode of AK
12. Presenting (at time of potential inclusion) a strong indication for immediate RRT
1. oligoanuria for more than 3 days
2. Alert criteria
13. Under cardiopulmonary bypass
14. Included in another clinical trial on RRT modalities

Result:

1. early group:
2. Late group: 157 receiving RRT ⇔ 101 w/o RRT, and the number in the late group with RRT are below:

3. The patients’ condition at the timing of RRT initiation:

Metabolic abnormalities were more marked in the delayed strategy group than in the early strategy

4. Whether there is different modality or condition between the two group?

	Early group	Late
deaths at day 60	150	153
mortality at Kaplan-Meier	48.5%	49.7%
overall mortality at D60	49.1%

6. Post hoc exploratory analysis

	Early	Late - RRT	Late + RRT
D60 Mortality	48.5%	37.1%	61.8%
Baseline severity SOFA (Med)	11	10	12
Adjustment for severity	non-significant
The # of days free from RRT	lower  (17)	higher (19)
CRBSI	higher (10%)	lower (5%)
Hypophosphatemia	higher (22%)	lower (25%)
Hemorrhage of other etiologies (other than GIB or dialysis catheter)	lower (0.3%)	higher (4%)
Adequate diuresis w/o RRT		Earlier

Discussion

1. No survival benefit was observed with the delayed strategy of RRT
1. The recovery of renal function, as marked by diuresis, was more rapid and catheter relted infections occurred less frequently in the delyaed-strategy group than in the early-strategy group
2. Lengths of stay in the ICU and in the hospital were similar in the two groups
1. Allowing time for renal funciton recovery did not lead to prolongation of the stay in the ICU
3. This study is not generalizale => > 50% iHD first + only 30% CRRT alone

Limitations:

1. The power of the study to distriguish a significant difference in mortality could be questioned
2. Not using Kt/V to evaluate the dose of RRT => However, the study keep serum urea low during therapy
3. The study group is “advanced” AKI => may not be generalizable to patients with different KDIGO stages of AKI
4. 有些人可能會把這個研究在接受Late-strategy這組的高致死率詮譯作一個”late strategy”有害的效果 （deleterious effect）。然而，在接受到”late RRT"的這組病人（比起不是接受”late RRT”的那一組）明顯有比較差的疾病狀況；並且進一步地對疾病嚴重程度加以校正來看的話，會發現所觀察到的crude difference是受到干擾的（was confounded)。

" Our study should not be interpreted as suggesting that a “”wait and see” approach is safe for all patients.” => Careful surveillance is mandatory when deciding to delay RRT in patients wi severe AKI….

Conclusion:

No significant difference in mortality with a strategy of delayed initiation as compared with early initiation of RRT.

Hepatojugular reflux and Kussmaul sign

Hepatojugular reflux and Kussmaul sign

DeGowin's Diagnostic Examination, 9/e, p.387

These phenomena are caused by inability of the right heart to accommodate increased venous return.

Position the patient so the blood column is just visible in the jugular veins above the clavicle.

With the patient breathin normally, place the right hand on the right upper abdominal quadrant and press firmly upward under the costal margin for at least 10-15 seconds.

The hepatojugular reflux sign is present if the top of the jugular venous column in the neck rises and persists as long as the abdominal pressure is continued.

Kussmaul sign is present when the jugular venous column fails to collapse during inspiration due to increased intraabdominal pressure created by the diaphragm during inspiration.

The hepatojugular reflux sign is most commonly seen with eearly right heart fialure.

Both signs may be seen with severe right heart failure, constrictive pericarditis, and right ventricular infarction.

2016 AJKD--Pathophysiology of Renal Tubular Acidosis: Core Curriculum 2016 -- Hyperkalemic RTA (type 4)

Topic: Pathophysiology of Renal Tubular Acidosis: Core  Curriculum 2016 -- Hyperkalemic RTA (type 4)
整理	內容 a defect in regeneration of HCO3 secondary to lack of adequate urinary NH4 => most common: hypo-aldosteronism w/ hyperkalemia => pesistent hyperkalemia without obvious cause (eg, kidney failure, use of K supplements, or K-sparing diuretics) hypo-aldosterone: hypo-reninism w/ kidney dz, Or a defect in RAA pathway Normal or high aldosterone in hyper-K RTA => the defect is in response to aldosteone: patients on ENaC blocker Hyper-K impair NH4 excretion: intracellular alkalosis (lumen K into PTC exchange for Na/H => inhibit ammoniagenesis 透過NKCC2抑制NH4在thick ascending limb of loop of Henle的reabsorption (K和NH4 compete for the same site on this transporter) => medullary NH4 absorption decrease Hereditary hyperkalemia RTA vs. Acquired hyperkalemic RTA Hereditary: Decrease in aldosterone synthesis (congenital isolated hypoaldosteronism or pseudohypoaldosteronism type 2), DCT NaCl absorption increase => 2nd hyperaldosteronism, Resistance to aldosterone action => type 1 pseudohypoaldosteronism Acquired: secondary to hyporeninism: CKD due to DKD or CIN Pirmary adrenal insufficiency can result from autoimmune adrenalitis, infectious adrenalitis (eg, HIV), and other disorders Severely ill patients due to unknown mechanisms Obstructive uropathy: impaired H and K secretion in CD (可能Urine pH > 5.5 when acidemia) Drugs: K-sparing diuretics, antibiotics (TPM and pentamidine), NSAID, CNi, Angiotensin inhibitors, Heparin/LMWH (附圖) Dx: document low NH4 + K excretion: UAG + UOG Urine pH < 5.5 (例外：obstr. uropathy, urine pH>5.5) Low urien K excetion: TTKG + Urine K/Cre ratio Drug screen serum Aldosterone + renin: hypo-aldo +/- hypo-renin Tx: Short-term: Normalize serum K => H+NH3 secretion增加改善metabolic acidosis + 增加PTC glutamine代謝，然後增加HCO3的產生 try to correct metabolic acidosis directly if failure to the 1st method Long-term: Hyper-K in P’t w/ Hyper-K RTA DC all drugs affecting K Restrict dietary K Control Hyperglycemia Tx metabolic acidosis Tx volume depletion Use loop diuretics (排酸？） Mineralocorticoids Kayexalate
摘要