Acid and Base Balance and Imbalance

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Acid-Base Imbalances
pH< 7.35 acidosis
pH > 7.45 alkalosis
The body response to acid-base imbalance is called compensation
May be complete if brought back within normal limits
Partial compensation if range is still outside norms.

Compensation
If underlying problem is metabolic,  hyperventilation or hypoventilation can help : respiratory compensation.
If problem is respiratory, renal mechanisms can bring about metabolic compensation.

Acidosis
Principal effect of acidosis is depression of the CNS through ↓  in synaptic transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes -Disorientation,coma ,death

Alkalosis
Alkalosis causes over excitability of the central and peripheral nervous systems.
Numbness
Lightheadedness
It can cause :Nervousness,muscle spasms or tetany ,Convulsions ,Loss of consciousness,Death

Respiratory Acidosis
Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg.
Hypercapnia – high levels of CO2 in blood
Chronic conditions:
 Depression of  respiratory center in brain that controls breathing rate – drugs or head trauma
 Paralysis of respiratory or chest muscles
 Emphysema
Acute conditons:
Adult Respiratory Distress Syndrome
Pulmonary edema
Pneumothorax

Signs and Symptoms of Respiratory Acidosis
Breathlessness
Restlessness
Lethargy and disorientation
Tremors, convulsions, coma
Respiratory rate rapid, then gradually depressed
Skin warm and flushed due to vasodilation caused by excess CO2

Acute Compartment Syndrome

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An increased pressure within enclosed osteofascial space that reduces capillary per-fusion below level necessary for tissue
viability; the underlying mechanism is:
- increased volume within space
- decreased space for contents
- combination of both

Etiology
Trauma with bleeding/swelling
Bleeding disorders
Burns
Tight wraps
Traction
Surgical positioning
Pneumatic antishock garment
Reprefusion swelling

Pathophysiology:
Increased compartment pressure leads to increased venous pressure which decreases A-V gradient resulting in muscle and nerve ischemia.

Variables to Consider
Vascular tone
Blood pressure
Duration of elevated pressure
Metabolic demand of tissue
Lowered ischemic threshold of damaged muscle

Myoglobinemia
Released in high levels at reperfusion
Toxic to glomeruli
Metabolic acidosis & hperkalemia
Together lead to:Renal failure,Cardiac arrhythmia & failure,Hypothermia and Shock

Diagnosis
Clinical exam: the Ps(Pressure,Pain,Paresthesia,Paralysis,Pallor,Pulselessness)
Compartment pressures
Laboratory tests-CPK and Urine myoglobin


Causes / Risk Factors for Obstructive Sleep Apnea
Obesity, Obesity, Obesity
Increasing age
Male gender
Structural abnormalties
Tonsillar hypertrophy, nasal pathology
Alcohol, smoking and family history

Up to 90% of adult patients with OSA are obese

Obstructive Sleep Apnea is defined as a cessation of airflow for more than 10 seconds despite continuing ventilatory effort, 5 or more times per hour of sleep and a decrease of more than 4% in SaO2.

What Happens with Normal Sleep?
4 to 6 cycles of N-REM sleep followed by REM sleep
4 stages of N-REM with progressive slowing of EEG
Stage 3 and 4 N-REM and REM are very deep levels of sleep
Progressive generalized loss of muscle tone
Restorative periods of sleep
Progressive decrease in muscle activity and resultant increase in upper airway resistance.

Airway Collapse
Occurs with loss of muscle activity
Increased subatmospheric pharyngeal pressure
MRI reveal anterior and lateral wall collapse

Obesity Effects Airway Anatomy Adversely
Inverse relationship between obesity and pharyngeal area
Fat deposits in the uvula, tongue, tonsillor pillars, aryepiglottic folds and lateral pharyngeal walls.


Propofol Infusion Syndrome

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PROPOFOL INFUSION SYNDROME
SUDDEN ONSET OF MARKED BRADYCARDIA, RESITANT TO TREATMENT,PROGRESSING TO COMPLETE HEART BLOCK
LIPEMIC PLASMA
CLINICALLY ENLARGED LIVER
METABOLIC ACIDOSIS WITH A BASE DEFICIT OF > 10 MMOL/L ON AT LEAST ONE OCCASION
RHABDOMYOLYSIS OR MYOGLOBINURIA

Propofol marketed in the USA since 11/1989.
PRIS has been described in both children and adult patients sedated with propofol.
FIRST CASE REPORTS- 1992

FDA Investigation of Deaths associated with Propofol
Reviewed reports of death with propofol as the suspect drug: pediatric pt(≤ 16y) and adults(>16y) for non-procedural sedation.
Time period= Nov 1989-Apr 2005.
Strict definition:
Metabolic acidosis and/or rhabdomyolysis with progressive cardiac failure US deaths for Nonprocedural sedation reported to the FDA

Case Report
2yo boy PICU s/p shot in the head with an air gun pellet.
Intubated and ventilated for right sided cerebral edema and rim of subdural blood.
Sedated with propofol rate of 4-5.4 mg/kg/h. over 72 h.
Day 4   
 oliguria, increase in K+,BUN, Cr and then sudden, persistent bradycardia(HR= 28).
Propofol stopped, trans-venous pacer placed, restored HR but had persistent acidosis.
Diagnosis: PRIS- started dialysis. Complete recovery.

Cholesteatoma

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16 year old female with left-sided otorrhea for two months
  • Otorrhea is yellow and foul-smelling
  • Otorrhea has not resolved with otic drops
  • Occasional dizziness
  • No fever
  • Otalgia has subsided
  • Intermittent unilateral tinnitus
  • Hearing loss
Physical Exam
Weber localizes to left
Rinne
AC > BC AD
BC > AC AS
Facial nerve intact
No nystagmus
Otherwise - within normal limits

Differential Diagnosis
  • Jugular bulb anomalies (high riding bulb, dehiscent jugular bulb, and jugular bulb diverticulum), aberrant internal carotid artery (ICA), hemangioma, persistent stapedial artery
  • Otitis Media, otitis externa, malignant otitis externa, tuberculous otitis
  • Tympanosclerosis
  • Granulomatous Diseases (a.k.a., Wegener’s granulomatosis)s
  • Osteoradionecrosis
  • Retained PE tube, Foreign Body
  • Cholesteatoma, paraganglioma / glomus tympanicum tumor, schwannoma, adenoma, endolymphatic sac tumor, cholesterol granuloma, polyps, adenocarcinoma, squamous cell carcinoma, adenoid cystic carcinoma
  • Cholesteatoma, encephalocele
Congenital or Acquired Cholesteatoma?
Congenital Cholesteatoma _Criteria
White mass medial to normal tympanic membrane
Normal pars flaccida and pars tensa
No prior history of otorrhea or perforations
No prior otologic procedures


Puberty

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It is a physiological phase lasting 2 to 5 years,during which the genital organs mature.The first sign of pubertal development is usually breast growth (thelarche), followed by appearance of pubic hair (pubarche), then (axillary hair), then (menarche).

Adrenarche
means increased activity of the suprarenal cortex at puberty with increased production of adrenal androgens which lead to appearance of pubic and axillary hair.

Cause of puberty:
During childhood , the hypothalamus is extremely sensitive to the negative feedback exerted by the small quantities of estradiol & testosterone produced by the child's ovaries .
As puberty approaches , the sensitivity of the hypothalamus is decreased and subsequently , it increase the pulsatile GnRH secretion .
The anterior pituitary responds by progressive secretion of FSH and LH associated with increased secretion of growth hormone .
The ovaries respond to the increase Gonadotrophin secretion by follicular development & estrogen secretion .
Estrogen causes development of the genital organs and the appearance of the secondary sexual characters .
With increased estrogen secretion , menarche and cyclic estrogen secretion occurs .

Factors affecting the initiation of pubertal development :
1 - Height and weight ratio (nutritional factors).
2 - Maturation of the hypothalamus .
3 - Increased neurotransmitter output in CNS .
4 - Onset of adrenal androgen activity 

FEMALE PRECOCIOUS PUBERTY
It means menarche or appearance of any of the secondary sexual characters before the age of 8 years.
1 - True precocious puberty
It is due to increased production of pituitary gonadotrophins.
2 - False(pseudo-precocious puberty)
It is of peripheral origin.
It is due to secretion of sex hormones; (estrogen or androgen) which is not dependent on pituitary gonadotrophins as in case of estrogenic or androgenic ovarian tumors.
3 - Incomplete precocious puberty .
In this case only one pubertal change as breast development is present before the age of 8 years without the presence of any other pubertal changes and in absence of increased estrogen production.
The other pubertal changes occur at the normal age.


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