ACID / BASE - Home | Stanford Medicine
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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