ACID / BASE



ACID / BASE

#1 METABOLIC ACIDOSIS

Winter's 1.5 (HCO3-) + 8 +/- 2 = Pa CO2

o Anion Gap acidoses:

prodn: ketones, lactate

ingestion: salicyllate, methanol, Et glycol

elimination: renal failure, phosphates, sulfate

prox tubule: HCO2- resorbtion

dist tubule: H+ secretion, Aldo activity

o Non AG: HCO3- matched by incr Cl-

*GI tract loss( diarrhea, laxative, cholestyramine, CaCl2, MgCl2, ileal conduit *other: hyper PTH, diamox

o RTA Prox: Urine pH often > 5.5 also see problems with other substances handled by prox tube ( glucose, AAs)

o Distal ph Always > 5..5

#2 METABOLIC ALKALOSIS

o Chloride sensitivie:

(vomiting , NG tubes , hypovolemia--kidney tries to minimize HCO3- and Na losses, diuretics, villous adenoma (KCl diarhea), post hypercapnic (overshoot alkalosis),

-urine Cl- < 20 meq/L

o Chloride resistant

-mineralocorticoid excess (Na resorbed, H out, volume expanded)

-re-feeding. Ketones and lactae metab. to HCO3-

- post oraganic aciosis, similar to refeeding, worse if HCO3- given

o ANALYTIC METHODSo

compare HCO3- and d Anion gap. If same, simple dissorder. If dHCO3- is less than d AG, then maybe a mixed Alk / Acidosis

- hypoalbunimeia may obscure an otherwise wide anion gap.

BE; change in acid/ base ( in nM) of whole blood needed to restore plasma pH to 7.4 at a pCO2 of 40mmHg.

Anion gap: main value is in identifying a combined chronic resp acidosis + acute metabolic acidosis.

ANTIDOTES

Acetaminophen:

Antidote - Acetylcysteine

Dose - 140 mg/kg PO

Arsenic, Mercury, & & Gold

Antidote - BAL

Dose - 5 mg/kg IM

Atropine

Antidote - Physostigmine Dose - 0.5 to 2.0 mg/kg

Benzodiazapines

Antidote - Flumazenil

Dose - 0.2-1 mg IV

Carbon Monoxide:

Antidote - oxygen

Cyanide:

Antidote - Amyl nitrite Pearls q2min then

Sodium nitrite 10 ml

of 3% sol over 3 mins IV

Ethylene glycol & Methanol:

Antidote - Ethyl alcohol

Dose - 1 ml/kg of 100% in glucose then dialysis

Iron

Antidote - Deferoxamine

Dose - 40-90 mg/kg

B-Blockers

Antidote - Glucagon

Dose - 5 mg/hr infusion

Calcium channel blockers

Antidote - Calcium chloride Dose - Bolus 60 mmol over 30 mins

Lead

Antidote - Calcium disodium versanate

Dose - 1 amp/250 D5W over 1hr

Methemoglobin

Methylene blue 2mg/kg

Nitrites

Antidote - Methylene blue

Dose - 0.2 ml/kg of 1% soln over 5 min

Narcotics

Antidote - Naloxone Dose - 0.4 to 0.8 mg

Organophosphates

Antidote - Atropine

Dose - 0.5-2 mg

and/or

Antidote - PAM

Dose - 1 g IV

Aspiration

recumbent: post segment of upper lobes

upright: basal lower lobes

*comm acquired: s. pneumo, s. aureus, H. influenza

*hospitalized: GNR, psuedomonas, enterobactracae

Treatment: recomended for those likely to have GI tract colonized (SBO, on PPI, etc.) and for those whose symptome do not resolve within 48 hrs.

Evidence based criteria

1 randomizrd controlled, many

IIa at least one RCT with comp. criteri

IIb one RCT meeting some criteria

III at lrasy one well-designrd trial

without randomization

IV opinions from authorities, case

reports, etc,

Fluid distribution (%TBW given)

TBW- 0.60 of wgt - - - of this:

0.67 intracellular (40% wgt)

0.33 extracellular (20% wgt) ,

of ECFV:

0.25 vascular (5% wgt)

0.75 interstitial (15% wgt)

Glascow Coma Scale

•eyes

open spont 4

to verbal 3

to pain 2

no resp 1

•best motor response

obeys verbal 6

localizes pain 5

flexion withdrawl 4

flexion abnormal 3

extension 2

no response 1

•best verbal

oriented, conversant 5

disorinted, convers. 4

inappropriate words 3

incomprehensible sounds 2

no response 1

gluccocorticoid potencies

Gluccocorticoid (GC/ MC/ dose equiv)

hydrocortisone 1 1 20

prednisone. - 4 0.8 5

solumedrol - 5 0.5 4

dexameth 25 0 0.75

betameth 25 0 0.6

Gram Stain

Staph--GP clusers

Strep--GPC occ rods

Pneum--GP diplo, lancet, some chains

Lactose fermenting:

STRONG: E Coli, Enterobacter, Klebsiella

WEAK: Citro, Providencia

NOT: Proteus, Slmonella, Shig, Pseudo

HYPEROSMOLAR NONKETOTIC DIABETIC COMA (HNDC)

DESIGNATIONS:

Also termed hyperosmolar coma, nonketotic hyperosmolar syndrome, and severe nonketotic hyperglycemic hyperosmolar syndrome.

DEFINITION:

HNDC is a state of extreme hyperglycemia, marked dehydration, serum hyperosmolarity, altered mental status, and absence of severe ketoacidosis (Ferri, 1991). The absence of severe ketosis distinguishes it from DKA.

PROFILE:

The patient is often a debilitated or elderly diabetic with impaired or no ability to communicate thirst over a 1-2 week period of osmotic diuresis.

Event leading to relative insulin deficiency

Hyperglycemia

Osmotic diuresis

Loss of large amounts of fluid and e'lytes

(water loss > e'lyte loss)

Prerenal azotemia

(inability to excrete large amouts of glucose)

Extreme hyperglycemia

(avg glucose level: 900-1000 mg/dl)

Hyperosmolarity

(avg serum osmolarity is 380 mOsm/L)

ETIOLOGY:

It is important to identify a precipitating cause of HNDC. In a series described by Rippe (1992), causes could be found in 16 of 20 cases.

1. Infections: pneumonia, sepsis, UTI

2. Metabolic abnormalities: new DM, noncompliance

3. Cardiovascular: MI, CVA

4. Drugs

a. Phenytoin and diazole: decreased insulin

b. Diuretics: excessive dehydration

c. Hypertonic alimentaion: osmotic diuresis

PATHOPHYSIOLOGY:

HNDC is relative insulin deficiency without ketosis. Pts have decreased levels of free fatty acids as compared with DKA. This supports the idea that there is sufficient insulin to prevent accelerated lipolysis characteristic of DKA which leads to ketogenesis and ketoacidosis. Ketone concentrations are elevated, however, to the starvation range: 2-4 mmole/L. Other possibilities include increased malonyl CoA production secondary to increased activity of the Cori cycle, where circulating glucose is converted to lactate in the liver for gluconeogenesis; from lactate comes malonyl CoA. Glucagon resistance may also contribute to decreased production of ketones.

SYMPTOMS:

Include polyuria, mental obtundation, SZ's, N/V. No acetone breath.

PHYSICAL EXAM:

1. Dehydration signs: decreased skin turgor, dry mucous membranes, sunken eyes

2. Neural deficits: reversible hemiplegia, focal SZ

3. Orthostatic hypotension, tachycardia

4. Evidence of a precipitating factor

LABORATORY:

1. Hyperglycemia: >600 mg/dl: often well over 1000 mg/dl

2. Hyperosmolarity

3. Na: may be low, normal, or elevated. More severe cases involve nl or high Na since serum Na has to be corrected when hyperglycemia occurs: for every 100 mg/dl increase in glucose above nl, Na is corrected 1.6 mEq/l, 2 mEq/l if there is accompanying dehydration.

4. K: low, nl, or elevated

5. HCO3: decreased (avg 17 mEq/l)

6. Avg pH = 7.26

7. Elevated BUN (60 - 90 mg/dl)

8. Decreased Ca, Mg, and P

TREATMENT:

1.Vigorous fluid replacement

2. Replace electrolytes

3. Correct hyperglycemia

a. vigorous hydration will decrease glucose 20 /hr

b. Insulin, 2-5 U/hr by IV

4. Treat precipitating causes

5. Monitor vitals, e'lytes, U. O., mental status changes, insulin infused, and fluids administered.

Infections after BMT

0-30 days- risk factor= neutropenia. Fungal and bacterial pneumonias, HSV, candida, Gram pos and Gram neg bacteria

30-90 days- risk factor= acute GVHD + therapy.

Interstitial pneumonias, CMV, aspergillus

90 days- 12 months- risk factor= chronic GVHD.

Bacterial and respiratory virus pneumonias, VZV, encapsulated bacteria

Prophylaxis in BMT patients:

1) PCP- TMP/SMX from engraftment x3-6 mos when ANC>1000 OR if chronic GVHD as long as immunosuppressants given. Alternative: aerosolized pentamapine

2) fungal prophylaxis- consider fluconazole or low-dose ampho B. Fever and neutropenia x3-5 days without response to broad-spectrum abx should get ampho (0.5-1 mg/kg/d)

3) CMV-

a) allo, CMV (-) donor & recipient, strict CMV (-) blood products- no prophylaxis

b) allo, CMV (+) donor or recipient: IVIG (500 mg/kg q2wx3 mos) PLUS blood, urine, throat cx qwk x 120d. (+) cx- ganciclovir + gamma globulin

c) autologous and (-) recipient- use (-) blood products.

Liver--misc

serum-ascites albumin gradient:

>11g/dl--portal htn, sterile cirrhotic, liver mets, CA

< 11g/dl TB, peritonitis, carcinomatosis of perit.

SBP: 40, PaO2 < 60, Pa CO2 > 45, likely RV

falure or resp failure

Pulm function 2

plasmapharesis or IVIG, no better with steriods

intubate if VC < 15ml/kg or trending that way

Poor prognosis:

age > 60

full progression to intub in < 7 days

decr motor amplitude on EEG

complications

delay in treatment

Myesthenia Gravis

occular, bulbar

Rx: corticosteriods plus plasma exchange > IVIG

look for related autoimmune pathology: Thyroid, adrenal, etc.

Cholinergic Crisis::SLUDGE

salivation

lacrimation

urination

defication

GI cramps

emesis

pinpoint pupils, wheezing, badycardia, coma

Cirtical Illness Polyneuropathy:

Thought secondary to SIRS, has both mmotor and sensory components, and can last for months

Acute quadraplegic neuropathy:

Motor only, secondary to NMBA, steriods, cn also have a myopathic component

oPost Cardiac Arrest (hypoxic ischemic) injury

Prognosis: presence of 4 risk factors on day 3 of coma predicts 96% mortality at 2 months:

Abnormal brainstem fx (any test)

No w-d to pain

No verbal response

Creatinine level > 1.5 mg/dl

age > 70

o Skin Infections

impetigo skin

ecthyma

erysipelas

cellulitis sup faschia

Nec Faschitis sub Q --> deep faschaial plane

1) fulminant with cutaneous exudate and hemorrhage

2) invisble with either anesthesia, or pain exceeding physical findings. Horizontal blood vessels not disupte

Time of surgerry mortality

< 24 hrs 6%

> 24 hrs 25 %

MRI T2 may is great at differentiating cellulitis vs. Nec Fash, but it should not delay surgical exploration if suspicion exists

Radiocontrast

• 0.45 NaCl 1ml/ kg/ hr for 12 hrs before and 12 hrs after procedure

• N-acetyl cysteine 600 mg PO bid day before and day after procedure + NaCl as above.

all protocols encourage to drink if thirsty

Ramsey Sedation Scale

1 anxious, agitated, restless

2 cooperative, tranquil

3 responds to comands

4 asleep but brisk response to voice or glabellar tap

5 asleep, sluggish resp to stimuli

6 asleep, no response

Seiz

control undeirlying

establish cv resp stability

look for rhabido

hyperthermia

dehyd

acidosis

arrythmia

pathophys

incr CVP PAP MAP

25-30 min later you get cmro2 cbf mismatch w/decr oxygen delivery to cytochrome system.

Excitotoxic fx then become problema tic

Skin rash and pressure ulcers

Drug rash:

1) morbilliform, cephalocaudal progression

2) erythema multiforme: target lesions, central bulla or necrotic center; if oral involvement, it's Stevens johnson.

3) Toxic epidermal necrolysis: extensive epidermal loss (sulfonamides, PCN, anticonvulsants)

4) vasculitis

Life threateening Dissorders:

1) Purpura fulminans-- hemorrhagic infarction and necrosis of large areas of the skin, cause is unknown but is related to infections and disturbances in clotting

2) Ecthyma gangrenosum (pseudomonal infs.)Roundm indurated red to purpoe macules or plaques, cellulitis

Pressure ulcer risks:

physical and mental illness, age, bowel or blad incont.,

Best Rx: moist wound care, surg. consultation if III, IV

Stroke

**presentation **risk

Stroke 9% for 5 years

TIA 10% for first year

6% for each sub. year

Asymptomatic

soft plaque (high) 10% per year

Ulcerated Plaques 7.5% per year

Temp Regulation and Clinical Syndromes

#1 Radiation: can take place in a vaccuum; heat can be absorbed, transmitted, reflected. Temp loss dT4. Undraped pt.

#2 Convection: fluid motion -

#3 Evaporation: predom. mode when T > 37C.

#4 Conduction: 2 bodies in contact

> 35 hypothermic

32-35 mild (incr HR, resp, diuresis, shiverrring, dMS)

28-32 mod (decr CO, ventilaiton, CNS, loss of shiv)

< 28 severe (arrryth, p. edemma, circ. collapse)

Heat exhaustion

Heat stroke (HE + CNS dysfunction)

exertional--exerc. w/ high temp, humidity

classic--prro thermoreg. cannot cool self

NMS (bromocryptine 2.5-7.5 po q8, Dnatrolene)

Transfusion reactions

*Febrile reactions:

donor WBC react with pt. serum (leukoagglutanins) (1/1-200)

*Allergic: mild (1/33-100)

*IgA deficient have anti-IgA antibodies

*Volume overload (1/100)

*Acute lung injury: donor Igs react with host WBC,

the opposite, or donor cytokines (1/5,000)

*Deaths

80% ABO incompatible (1/12-33,000)

15% from ALI

*Infectious/ septic (1/2000-20,000 for platelets)

Vasculitis

Small Vessel

skin only--benign leukocytoclastic angiitis

skin plus visceral involvement

Henoch-schonlein purpura

Mixed cryoglobulinemia

assoc with conn tiss dz, malig.

hypocomplement vasculitis

involving the panniculus

erythema nodosum

weber-christian disease

Medium sized vessels

skin only

livedo reticularis

subcutaneous nodules

systemic illnesses

polyarteritis nodosum

allergic granulomatosis (Churg Strauss)

Wegeners

lymphamatoid granulomatosis

Large vessel vasculitis

takayasus arteritis

giant cell, polymyalgia rheumatica

assoc with spondyloarthropathies

Vitamins and Neuropsychatiric Syndromes

Water-soluble vitamins: Coenzymes and prosthetic groups of enzymes involved in intermediate metabolism (see diagram).

NIACIN (NAD, etc; many enz.) Endogenous production from Trp.

Primary def: Corn-based diet

Secondary Chronic EtOH; Isoniazid (see B6 below)

Diagnosis: Urinary metabolites using HPLC

Pathol: Motor neuron damage, dorsal column degeneration

1. early def: decr. appetite, wgt loss, decr. conc'n, abd. aches

2. inter " : irritability, depression/fatigue, insomnia

3. advanced (pellagra )dementia, dermatitis, diarrhea, death

psychosis : mania, depression, delirium, paranoia, disorientation, confusion

encephalopathic syndrome: clouding of consciousness, cogwheel rigidity, uncontrollable suckling and grasping reflexes

B6, PYRIDOXINE (transaminases, conversion of Trp---> Niacin)

Deficiency: Poor GI absorption Complexes with Isoniazid, Hydralizine. Penicillamine; incr. physical activity, pregnancy

S/Sx: Weakness, irritability, seizures, periph. neuropathy, convulsions

B1 THIAMINE (HMP shunt, entry into Krebs, a-KG--> Succinate)

Uptake: folate dependent Storage: skeletal muscle

Deficiency: Chronic EtOH ER Dose: 50mg IV, 50mg IM/day

1. Early: weakness, neuropathy, headache, tachycardia

2. Late: wet beriberi (CV) high output heart failure

dry beriberi (Neural)

1. PNS: symmetrical decr. in motor, sensory and reflexes

+/- parasthesias; legs involved > arms

2. CNS: Wernicke's syndrome

ataxia opthalmoplegia

H-nystagmus global confusion, apathy

Korshakoff's psychosis:

impaired memory ---> amnesia

confabulation

B2 RIBOFLAVIN (FAD, FMN; many enz., redox reactions, MAO)

Sx: Personality deterioration Dermatitis, glossitis

Retarded intellectual development

Dx. RBC Glutathione reductase

Conversion of B2 to FMN (flavokinase) inhibited by a number of common medicines: chlorpromazine, tricyclics, adriamycin

B12 CYANOCOBALAMIN/ FOLIC ACID (DNA synth, methionine synth, FA synth/ myelin synthesis)

Mental s/sx--frequent irritability apathy somnolence

suspicious unstable depressive psychosis

Dementia--rare presentation

Peripheral NS (subacute combined degeneration of the spinal cord) : weakness, parasthesias--> unsteady gait--> stiff movements

loss of vibratory sense, defecits are classically symmetrical-- asymmetry

should make you consider other diagnoses

Hematologic abnormalities: Manifestations of impaired DNA synthesis

***these will often follow CNS manifestations of vitamin deficiency,

do not rule out B12 or folate deficiency because macrocytosis is absent !!

Fat Soluble Vitamins: A variety of biochemical roles--antioxidant (E), light sensor (A), coenzyme (K), and hormone (D). Syndromes of hypervitaminosis are possible.

Deficiency Excess

A Night blindness Weakness, headache

E Ataxia, peripheral neuropathy

D Tetany Weakness, lethargy

failure to thrive

Trace minerals: Common prosthetic groups, enzyme cofactors

Copper Excess (Wilson's disease)

Neural S/sx: Dystonic facies, upper extr.; unsteady gait, tremor and loss

of fine motor coordination, drooling, dysarthria

Psychiatric: Intellectual deterrioration, personality changes, unstable behavior, routine tasks become difficult, organic dementia indistingusihable from bipolar or schizophrenia.

Maganese deficiency

Ataxia, convulsions

Cromium deficiency (Cr complexes with nicotinamide to form "glucose tolerance factor," a factor required for proper binding of Insulin to its receptor).

Encephalopathy, neuropathy due to hyperosmolar ketotic coma

Vanadium (inhibitor of Mg-dependent ATPases; also said to stimulate adenyl cyclase)

deficiency produces edema

excess had been postulated to precipitate a manic depressive-type illness

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