Liver abscess

1. 1. LIVER ABSCESS BY- RAMYA DEEPTHI P VIJAY MARIE COLLEGE OF NURSING

2. 2. INTRODUCTION  Liver abscess are more common in developing countries.  Majority of
them are due to parasitic infestations- amoebic, echinococcosis.  It is rarely seen in
developed countries.
3. 3. Etiology I. Bacterial infections a. Pyogenci liver abscess b. Pyophlebitis abscess c.
Cholangitic abscess II. Parasitic infestations A. Protozoal disease a. Amoebiasis b. Malaria c.
Kala azar B. Helmenthic disease a. Ascariasis b. Liver flukes c. Echinococcosis (Hydatid disease)
C. Leptospirosis D. Syphilis
4. 4. PYOGENIC LIVER ABSCESS  Most liver abscess re of bacterial in origin.  Infecting
organisms are- 1. Garm negative bacteria- E. Coli, Pseudomonas Klebsiella, enetrobacter 
Route of entry to liver are- a. Portal vein b. Arterial supply c. Ascending infection from biliary
tract d. Direct invasion of liver from nearby source e. Penetrating injury f. Cryptogenic
(unknown)
5. 5. Morphology  Gross:  Depends on the cause of pyogenic liver abscess  Abscess may be
single or multiple  Vary in size from few millimeters to massive lesion  If single, abscess is
usually walled off by a thick fibrous capsule.
6. 6. Microscopic changes  Multiple neutorphilic abscess with areas of necrosis are seen n the
liver parenchyma.  Adjacent area shows pus, inflammation, congestion and proliferating
fibroblasts  Causative organism can be occasionally identified with special strains or when
material is cultured.
7. 7. Clinical features  Pain in liver origin- right upper quadrant  Fever  Tenderness 
Hepatomegaly  Rarely jaundice  Investigations reveal raised total leukocyte count with
neutrophilia  Elevated serum liver enzyme levels  Positive blood cultures.
8. 8. II. AMOEBIC LIVER ABSCESS  AMOEBIC LIVER ABSCESS IS MORE COMMON IN DEVELOPING
COUNTRIES.  However it is not as common as pyogenic abscess.  Pathogenesis is caused by
Entamoeba Histolytica.  It spreads form intestinal lesions  Parasite occurs in 2 forms-
Trophozoite and cystic form.  Cysts are more infective stages of the parasite and are found in
contaminated water and food.
9. 9. GROSS APPEARANCE:  Amoebic liver abscess are solitary, often found in the right hepatic
lobe.  Multiple abscess are found only in advanced cases.  Size of abscess vary  Centre
part of abscess contains necrotizing area filled with reddish brown, thick pus which resembles
anchovy or chocolate sauce.
10. 10. MICROSCOPIC CHANGES:  Necrotic area consists of degenerated hepatocytes,
inflammatory cell infiltarte, red blood cells, strands of connective tissue and necrotic debris. 
Trophozoites of amoebae are usually found in the necrotic area especially at the margins 
These cells resemble foamy macrophages and at times becomes difficult to distinguish them
from macrophages.
11. 11. Complications of amoebic abscess  Large abscess may rupture, penetrate the diaphragm
and enter into lung  Rupture into pleural cavity , peritoneal cavity or pericardia sac.
12. 12. III. HYDATID DISEASE  Hydatid disease is caused by the larval stage of small tapeworm
Echinococcus Granulosis.  It is common in sheep and occur in humans with close contact
with them.  Dog is the definite host.  Sheep, cattle and humans are intermediate hosts.
13. 13. Pathogenesis  Man acquires this infection by eating contaminated vegetables or water
and those handling dogs.  The embryo is liberated form the ovum in the small intestine of
man.  It gains access to blood stream and are carried to the liver by portal veins.  These are
trapped in liver where they grown into cysts.  This cyst grows very slowly, may rupture giving
multiple cysts and spreads to distant parts of the body.
14. 14. Clinical features  Uncomplicated hydatid disease remains for longer time silently and may
produce only dull ache in the liver region.
15. 15. Morphology  Hydatid cyst grows slowly and may reach a size of 10cm in few years. a.
Outer pericyst or adventitia:  Has fibroblastic proliferation, esinophils and giant cells. It later
forms as thick fibrous capsule b. Intermediate ecto cyst:  Which is composed of acellular
laminated hyaline material c. Inner endo cyst:  it is the innermot germinal layer consisting of
daughter cysts and hooklets which projects into lumen.
16. 16. complications  Rupture of cyst into peritoneal cavity, bile ducts and lungs causes
anaphylactic reaction  Fine needle aspiration is an absolute contraindication
INVESTIGATIONS  Peripheral blood smear  X-ray examination  serology
17. 17. Thank you…
1. . By Ashraf Okba Prof. of Internal Medicine Ain Shams University
2. 2. Overview Enviromental causes Hepatic Injury Hepatitis virus Alcohol Drugs and toxins
Recovery Fulminant hepatic failure Chronic persistent hepatitis Necrosis cirrhosis
Herritage/Genetic causes Hepatic Failure hepatic insufficiency Hepatorenal syndrome Hepatic
Encephalopathy Triggers
3. 3.  Cirrhosis is a liver disease characterized by extensive fibrosis with regenerative nodule
formation, and distortion of liver structure.  It is referred to as the end stage of many chronic
liver diseases.  The progression of a specific chronic liver disease to cirrhosis can take many
years and is dependent upon many factors such as the severity of the liver disease, lifestyle,
and overall health of the individual.  Cirrhosis is an irreversible condition that also has serious
complications 3
4. 4. Chronic Viral Hepatitis  Hepatitis is the inflammation of the liver caused by hepatitis B or C
virus Chronic Alcoholism  Excessive alcohol intake is the leading cause cirrhosis in the
United States.  Chronic alcoholism is the most common cause of steatosis, a condition
characterized by fat build up in the liver. . Nonalcoholic steatohepatitis (NASH)  This
condition exhibits the same characteristics of steatosis that inflames the liver. However, it is
not caused by alcohol consumption. This condition often exists in conjunction with other
health issues such as obesity, diabetes, and coronary artery disease. Bile Duct Disease 4
5. 5. A) Compensated cirrhosis Body still functions fairly well despite scarring of the liver. Few or
no symptoms. Symptoms of compensated cirrhosis 1. Fatigue and loss of energy 2. Loss of
appetite and weight loss 3. Nausea or abdominal pain 5
6. 6. B) Decompensated cirrhosis severe scarring of the liver disrupting essential body functions ,
develop any serious symptoms and complications Symptoms of decompensated cirrhosis: 1.
LL. edema 2. Ascites 3. Portal hypertension 4. jaundice 6
7. 7. HEPATIC FUNTION CLINICAL MANIFESTATIONS  Body’s metabolism 1．Carbohydrate
metabolism 2． Protein metabolism 3．Lipid metabolism 4. Water and Electrolyte
metabolism 5．Hormone metabolism  Blood coagulation  Biotransformation and
detoxifcation  Immunity  Secretion and excretory function  Metabolism dysfunction
1．Hypoglycemia 2．Hypoalbuminemia 、high ammonia、 3．Fatty liver、decreased
plasma cholesteryl ester 4． Disorders Water and Electrolyte metabolism 5. High
estrogen，spider angioma 、 liver palms etc.  Bleeding tendency  Intoxication  Infection 
Jaundice
8. 8. Palmar erythema Spider navei
9. 9. Conditions in which the liver functions fall below the normal ranges. The symptom include
jaundice, bleeding, secondary infection, renal dysfunction and hepatic encephalopathy .
Hepatic insufficiency Hepatic failure Hepatic failure is a terminal stage of hepatic insufficiency.
Hepatic encephalopathy and hepatorenal syndrom are the primary clinical manifestations.
Severe hepatic insufficiency may cause liver failure or death.
10. 10. HEPATORENAL SYNDROME Hepatorenal syndrome is the development of a reversible and
functional renal failure in patients with severe liver diseases in absence of any other identified
cause of renal pathology. It is characterized by a marked decrease in GFR and renal plasma
flow.
11. 11. Pathophysiology Of Hepatic Cirrhosis
12. 12.  Normally, hepatocytes are capable of considerable regeneration.  However, chronic
damage (from viral infection, heavy alcohol consumption, trauma and other factors) can lead
to scarring.  This scarring is referred to as fibrosis.  Formation of scar tissue is a normal
bodily response to injury. The injury or death (necrosis) of hepatocytes stimulates
inflammatory immune cells to release cytokines, growth factors, and other chemicals.  These
chemical messengers direct support cells in the liver called hepatic stellate cells to activate
and produce collagen, a fibrous connective tissue that gets deposited in the liver. 13
13. 13.  In fibrosis, excessive scar tissue builds up faster than it can be broken down and removed
from the liver.  If the disease progresses, it can lead to cirrhosis, a condition in which the liver
is severely scarred, its blood flow is restricted, and its ability to function is impaired.  The
nodular regeneration of the liver tissue, permanently alters the structure of the liver. 14
14. 14.  The major complications of cirrhosis are similar in both alcoholic and nonalcoholic
patients:  Portal hypertensive bleeding Increased blood pressure in the blood vessels
supplying the liver due to increased in vessel resistance. Portal hypertension leads to the
development of new veins called collateral veins, at the end of esophagus and at the upper
portion of the stomach. These collateral veins become varicose veins that are prone to
bleeding.  Ascites  Excess fluid in the peritoneal cavity  Hepatic encephalopathy  Mental
confusion , change in the level of consciousness  Hepatocellular carcinoma Most common
liver cancer 15
15. 15. 2010 年 10 月 22 日 Definition of Hepatic Encephalopathy Hepatic encephalopathy (HE) is a
complex, potentially reversible disturbance in CNS that occurs as a consequence of severe liver
diseases. It is characterized by neuropsychical manifestations ranging from a slightly altered
mental status to coma.
16. 16. The West Haven criteria of altered mental state in HE (In patients with cirrhosis and overt
encephalopathy) Stage 0. Lack of detectable changes in personality or behavior. Asterixis
absent. Stage 1. Trivial lack of awareness. Shortened attention span. Impaired addition or
subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria or depression.
Asterixis can be detected. Stage 2. Lethargy or apathy. Disorientation. Inappropriate behavior.
Slurred speech. Obvious asterixis. Stage 3. Gross disorientation. Bizarre behavior. Semistupor
to stupor. Asterixis generally absent. Stage 4. Coma. THE AMERICAN JOURNAL OF
GASTROENTEROLOGY Vol. 96, No. 7, 2001 Staging
17. 17. A classification of hepatic encephalopathy was introduced at the World Congress of
Gastroenterology 1998 in Vienna. According to this classification, hepatic encephalopathy is
subdivided in type A, B and C depending on the underlying cause. Types Type A (=acute)
describes hepatic encephalopathy associated with acute failure Type B (=bypass) is caused by
portal-systemic shunting without associated intrinsic liver disease Type C (=cirrhosis) occurs in
patients with cirrhosis this type is subdivided in episodic, persistent and minimal
ncephalopathy
18. 18. PATHOGENESIS OF HE HE may be due to primarily to a failure of the liver to remove
adequately certain substances in plasma that have the ability, directly or indirectly to
modulate the function of the central nervous system. Several hypotheses have been proposed:
19. 19. PATHOGENESIS  The pathogenesis of HE remains poorly understood  HE in liver cirrhosis
is a clinical manifestation of a low-grade cerebral edema, which is exacerbated in response to
ammonia and other neurotoxins
20. 20. Ammonia intoxincation hypothesis False neurotransmitters hypothesis Amino acid
imbalance hypothesis The Gamma-aminobutyric acid hypothesis Synergistic actions of
multiple toxins Pathogenesis
21. 21.  Causes of elevated ammonia in hepatic inssufficiency 1）Decreased clearance of
ammonia 2）Increase production of ammonia in gstrointestinal tract  Intoxicaton of
ammonia on the brain 1）Impairment of energy metabolism in brain 2）Alteration of
neurotransmitters 3）Inhibiting action of nerve cells membrane Ammonia intoxincation
22. 22. Urea AANH3 NH3 NH3 Ornithine CitrullineArgininosuccinate  Urea NH3  Kidney Brain
Systemic circulation Liver Intestine Protal-systemic shunts Other tissues to produce NH3
1）Impairment of energy metabolism in brain 2）Alteration of neurotransmitters
3）Inhibiting action of nerve cells membrane
23. 23. False neurotransmisson hypothesis In hepatic dysfunction or formation of portal-systemic
shunt, some kind of amine elevated due to failure of hepatic deamination, and then filter into
central nervous system interferes with physiologic functions by competitively inhibiting
normal neurotransmitters (dopamine, norepinephrine) and favoring formation of false
neurotransmitters (octopamine, phenylethanolamine) ,which have similar structure but much
weaker activity than true neurotransmitters. The net physiologic result of such changes is
reduced neural excitation an hence increased neural inhibition.
24. 24. The aromatic amino acids (AAA), tyrosine,phenylalanine and tryptophan are increased in
liver disease whiletge branched amino acids (BCAA), valine,leucine and isoleucine are
decreased. The AAA are the precursors of false neurotransmitters. Amino acid imbalance
hypothesis
25. 25.  Plasma level of GABA In liver failure, a major resource of the increased plama GABA is
considered to be the intestinal bacteria and the intestinal wall. The permeability of the blood-
brain to GABA is increased in liver failure,if some of the GABAis not catabolized or taken up by
neurons,it may reach GABA receptors and augment GABA-ergic neurotransmission. Activation
of the GABA receptor increase neuronal membrane permeability to Cl- BY OPENING Cl-
ionophore, and Cl- enters the neuron causing membrane hyperpolarization.
Benzodizepines(BZ) recepter agonists increase the frequency of GABA-gate Cl- channel
openings. GABA and/or BZ receptor density increased Ammonia can augment the activity of
GABA-ergic neurons. Gamma-amino butyric acid hypothesis
26. 26. SYNERGISTIC ACTIONS OF MULTIPLE TOXINS Manganese: induce pathological changes of
astrocyte Mercaptans: inhibit the production of urea and Na+-k+- ATPase on neuron
membrane，disturbe the electron transport on mitochondria Short-chain fatty acids: inhibit
energy metabolism of the brain, and disturbe the post neuron potential Phenols: inhibite the
activity of many enzymes
27. 27. PATHOGENESIS  The accumulation of ammonia and other neurotoxins in the systemic
circulation is the main pathogenic factor in HE.  Normally, these neurotoxins are produced
(from gut bacteria) and absorbed from the gut and cleared by the liver.  When liver function is
seriously impaired (Acute or Chronic LF), these neurotoxins bypass the liver and gain access to
the systemic circulation, cross the blood-brain barrier, and accumulate in the CNS.
28. 28.  Unchanged ammonia traverses the BBB, and enter the parenchymal cells (especially
astrocytes), where it is converted into glutamine.  Glutamine in turn has osmolar activity and
increases the cell water content, contributing to cerebral edema.  Therefore, ammonia plays
the key role in the pathogenesis of HE by inducing astrocyte swelling and/or sensitizing
astrocytes to swelling by a heterogeneous panel of precipitating factors and conditions
29. 29. Glutamate L-glutamine Glutatrate GABA Citric acid Oxaloacetate Succinate NH3 ATP ADP
NAD NADH NH3 Pyruvic acid Acetyl-CoA Acetylcholine Choline    NADH NAD Toxicaton effect
of ammonia on brain tissue  NH3
30. 30.  Swelling of astrocytes produces reactive oxygen and nitrogen oxide species (ROS/RNOS),
which again increases astrocyte swelling and subsequently induces RNA oxidation that may
impair postsynaptic protein synthesis, which is required for memory formation and offers a
novel explanation for multiple disturbances of the neurotransmitter systems, gene expression,
motor and cognitive deficits observed in HE
31. 31.  and the energy supply to other brain cells is decreased.  Other waste products
implicated in hepatic encephalopathy include mercaptans , short- chain fatty acids and phenol
 Benzodiazepine-like compounds have been detected at increased levels as well as
abnormalities in the GABA neurotransmission system. 33
32. 32.  An imbalance between aromatic amino acids (phenylalanine, tryptophan and tyrosine)
AAA and branched-chain amino acids BCAA (leucine, isoleucine and valine) has been described;
this would lead to the generation of false neurotransmitters (such octopamine and 2-
hydroxyphenethylamine).  Dysregulation of the serotonin system, too, has been reported.
Depletion of zinc and accumulation of manganese may play a role 34
33. 33. Normal Liver diseases BCAA/AAA=about 3.5 (Fischer’s ratio) BCAA/AAA=about 1 (in a severe
condition) Increased amount of ammonia disposed of in the skeletal muscles Increased
amount of BCAA used as an energy source BCAA AAA AAA BCAA Metabolisms of BCAA and AAA
in Liver Disease 36
34. 34. Ammonia-glutamate metabolism in Skeletal muscle and brain BCAA BCKA  - Ketoglutarate
glutamate NH4+ glutamine 37
35. 35. PHYSIOLOGICAL FUNCTIONS OF BCAA • Energy source for the peripheral organ (e.g. skeletal
muscle) • Ammonia detoxification by glutamate and glutamine pathway. • Improve nitrogen
balance and elevate plasma protein level including albumin. 38
36. 36. • EAAs can't be produced by the body and can therefore only be obtained via the diet. •
Foods containing complete range of EAAs, approximately 40%, and termed as HBV (High
Biological Value), as Milk, cheese, yoghourt, beef, lamb, poultry, fish, and eggs. • NEAAs
produced by the body through "Amino Acid Pool", and containing foods are foods with LBV
"Low Biological value". As beans, peas, and nuts. • Patient with trauma, or surgery, or
recovering from burns or open wounds should be supplied with protein and energy. 39
37. 37. Essential & Non-essential Amino-Acids EAA NEAA Lysine Proline Phenylalanine Glycine
Valine (BCAA) Arginine (may become essentialduring specific disease states and is therefore
termed "semi- essential") Leucine (BCAA) Cystine Isoleucine (BCAA) Cysteine Threonine
Tyrosine Tryptophane Serine Methionine Aspartic acid Glutamic acid Alanine 40
38. 38. Glutamic acid GABA Metabolism  GABA GABA  Inhibit brain function
39. 39.  About 1/3 to ½ of hospitalizations for cirrhosis are related to HE  Patients with HE often
have other manifestations of end-stage liver disease ESLD, however HE can also develop as an
isolated manifestation of decompensate cirrhosis.  Hepatic encephalopathy may disable the
patient from employment, driving and self care.  HE usually signals advanced liver disease
and consequently is often considered a clinical indication for liver transplantation
40. 40. Types of hepatic encephalopathy
41. 41. Types of hepatic encephalopathy
42. 42.  GI bleeding  Infections: (UTI, chest, skin, SBP(Spontaneous Bacterial Peritonitis)) 
Constipation  Excessive dietary proteins  Electrolyte disturbance: (Hypokalemia,
Hyponatremia)  Superimposed liver injury: (acute viral hepatitis, drugs  Surgery  CNS
depressant drugs  HCC (Hepatocellular carcinoma)  Dehydration  Renal failure  TIPS
(Transjugular intrahepatic portosystemic shunt)
43. 43.  Transjugular intrahepatic portosystemic shunts (TIPS) are an established treatment in
the management of variceal bleeding and in a limited number of patients with refractory
ascites.  The incidence of hepatic encephalopathy increases in the presence of portosystemic
shunts
44. 44. Clinical stages/ grades (MCNA 2008)
45. 45.  Suspect in any liver disease patient presenting with mental changes  HE is usually
preceded by ppt factor  Asterexis = flapping tremors  Stage II  Weakens in stage III 
Disappears in coma
46. 46. NUMBER CONNECTION TEST  Used for > 50 years to assess mental performance  Simple,
readily available  Results influenced by age and level of education Source: Weissenborn et al.
J Hepatology May 2011 Time required HE Grade ≤30 seconds None-Minimal 31-50 seconds
Minimal - I 51 to 80 seconds I - II 81 – 120 seconds II - III Forced termination III Number
Connection Test Patient’s Name Date Completion Time Testers Initials Patient’s Signature
47. 47. MAJOR DIFFERENTIAL DIAGNOSIS  Seizures and focal neurological signs are uncommon
manifestation of HE warrants appropriate brain imaging  Structural brain damage : 
 Subdural hematoma !  Other metabolic encephalopathies:  Uremic  Hypoglycemia 
Ketoacidosis  Hypoxia  Thyroid dysfunction  CNS infections (meningitis, encephalitis) 
Ischemic brain disease (TIAs, Ischemic strokes)  CNS tumors
48. 48. INVESTIGATION  Overt HE from history and clinical examination  Diagnosis not clear or in
question  Blood ammonia level  Brain imaging (CT, MRI)  EEG  Psychometric tests (MHE)?
49. 49. CLINICAL EVALUATION  NH3 elevated in 90% of all HE but also at least marginally elevated
in 90% of all patients with cirrhosis  NH3 levels correlate (poorly) with HE Grade  EEG not
used routinely - Normal for stage 0 or MHE - Triphasic waves over frontal lobes that oscillate at
5 Hz for stage I,II,III - Slow delta wave activity in stage IV  MRI/CT typically only show findings
in Type A (fulminate liver failure) and Grade 4 HE Source: Ong JP, et al. Am J Med.
2003;114:188-93.
50. 50. Normal Results The normal range is 15 - 45 micrograms per deciliter (mcg/dL). What
Abnormal Results Mean Abnormal results may mean you have increased ammonia levels. This
may be due to: Congestive heart failure Gastrointestinal (GI) bleeding - usually in the upper GI
tract Genetic diseases of the urea cycle High body temperature (hyperthermia) Leukemia Liver
failure Low blood potassium level (hypokalemia) Metabolic alkalosis Severe muscle exertion
51. 51. Problem in bioassay of ammonia • Labile spontaneous determination + evaporation at
room temp  Venous blood ammonia correlates well with arterial ammonia when properly
assessed  Samples must be withdrawn in heparinized container, placed in ice and assayed
within 30 min
52. 52. CONCERNS  Normal blood ammonia level doesn’t support the diagnosis of HE 
Conversely, an elevated ammonia level in a comatosed patient doesn’t exclude a coexistent
condition.  However, markedly elevated blood ammonia (> 150 – 200 umol/l) strongly
suspicious of HE  Blood ammonia is moderately elevated in cirrhotic without HE
53. 53. Hepatic encephalopathy Management
54. 54.  European Society for Parenteral and Enteral Nutrition concluded the following: 
Cirrhotic patients tend to be hypermetabolic, and need higher than normal supply of protein to
achieve nitrogen balance.  Most patients tolerate a normal or even increased dietary protein
intake without risk of hepatic encephalopathy. ESPEN Consensus Review
55. 55. ESPEN Consensus Review  A modified eating pattern based on several meals and a late
evening snack, is useful.  In severe cases, AA should be supplied to meet protein
requirements.  Intolerant patients to the required protein intake, BCAA may be considered to
provide necessary nitrogen intake without detrimental effect on the mental state, or even
improving it.
56. 56.  Precipitating factors:  Dehydration  GI bleeding  Infection  Electrolyte disturbance 
Hypokalemia  Hyponatremia  Artificial liver support  Ammonia  ↓ production +
absorption  Diet  Lactulose + lactitol  Oral antibiotics  ↑ ammonia clearance  L ornithine
– L – Aspartate  Liver transplantation
57. 57. MANAGEMENT A) Precipitating factor  Dehydration:  Stop diuretics  IV physiologic saline
 GI bleeding:  Infection  SBP  UT  Chest  Electrolyte disturbance  Hypokalemia → IV k 
Hyponatremia → hypertonic saline (150 ml of 3% NaCl IV) (S. sodium < 125 mEq/L)  Any
episode of HE is considered due to end- stage liver disease ESLD only after exclusion of any ppt
factor
58. 58.  ↓ Production of gut ammonia 1- Diet  Excessive dietary protein can ppt HE  Patients
with compensated cirrhosis:  No restriction  Diet containing 1.2 gm protein/kg/ day is
Recommended
59. 59. Diet  HE episode →  Protein restriction to 40 gm/ day is advocated not more than 48
hours and then minimized  Prolonged protein restriction in HE → can exacerbate the catabolic
state of cirrhosis →release of AA and other nitrogenated byproducts from the muscles.
60. 60. Diet  Chronic HE  Vegetable proteins are better tolerated than animal proteins:  ↑
content of dietary fibers → natural cathartic  ↓ levels of AA acids→ false transmitters 
Supplementation with oral branched chain AAs → improves survival and QOL (expensive)
 61. 61. 2- Lactulose or lactitol (cathartics)  Lactulose (beta – galactosido fructose)  Lactitol (beta
– galactosido sorbitol)  Lactulose & lactitol Non absorbable disaccharides  Cathartic  ↓
colonic bacterial load  ↓ Gut ammonia production  Degradation by gut bacteria  Lactic acid
+ other organic A  Acidification of gut lumen  Inhibit ammoniagenic coliform bacteria
62. 62. LACTULOSE  Metabolized by colon bacterial flora to short chain fatty acids altering
luminal pH Lactic Acid - NH3 NH4 + Excreted in feces Lactulose Intestinal Flora
63. 63.  Lactulose Orally  30 ml/2-4 times/day (stage I, II) 3 – 5 loose motions  Lactulose Enema
 300 ml + 700 ml tap water / 4h (stage III, IV = coma) (massive ascites)  Many clinical trials
demonstrated the efficacy of lacutlose in the treatment of HE  However, one recent
metanalysis contradicts these trials and forces the use of antibiotics particularly rifaximin .
64. 64. 3- Oral antibiotics  They ↓ the concentration of ammoniagenic bacteria → ↓ production of
ammonia and other gut derived neurotoxins  Neomycin →250 mg/ 2-4 times/ day  Its efficacy
is ambigous .  Long term therapy → toxicity due to some systemic absorption  Metronidazole
+ oral Vancomycin are little studied
65. 65.  Rifaximin  non absorbable derivative of rifampin  550 mg orally TWICE DAILY  Studies
have demonstrated that rifaximin showed superior efficacy compared with lacutlose and
neomycin in HE as well as better tolerability than both drugs due to minimal absorption 
Concerns → cost ?
66. 66.  ↑ammonia clearance  L-ornithine – L-aspartate (LOLA)  Stable salt of 2 amino acids: 
L-ornithine  L-aspartate
67. 67. MANAGEMENT C) LIVER DIALYSIS  2 systems:  MARS:  molecular adsorbent recirculating
system  Albumin dialysis .  Prometheus: Fractionated plasma separation (FDPS) Introduced
2003  Both systems are capable of removing both water solved and albumin bound toxins
without providing synthetic functions.  Several clinical trials have shown that artificial liver
support, is able to improve HE in acute and acute on chronic liver fialure
68. 68. MOLECULAR ADSORBENT RECIRCULATING SYSTEM(MARS)  MARS is a device used to
perform albumin liver dialysis.  The basic technical concept is based on conventional HD  It
is a liver support system developed to support excretory liver function  It uses an albumin
enriched dialysate to facilitate the removal albumin bound toxin(ABT)
69. 69. USES OF MARS  Acute fulminant liver failure  Acute on chronic liver failure (acute
hepatorenal synd)  ALF with extensive liver resection for tumour  As temporary support in
spontaneous recovery following abalative liver surgery  Liver transplant pt with primary graft
dysfunction
70. 70.  Cirrhotic patients who develop severe HE have poor survival even with a fairly low MEID
score, therefore, this constitutes a clinical indication for liver transplant evaluation is the only
mode of therapy that tackles  the real cause of chronic HE which is the lack of functioning
hepatocytes

Hepatocellular carcinoma
1. 1. Presented by: Dr. Aleena Bhari Dr.Kawshik Ahmed Intern doctors, Surgery department Enam
medical college and hospital
2. 2. Anatomy of liver
3. 3. Surgical anatomy The Couinaud classification system divides liver into 8 independent
functional units (segements)
4. 4. Contd.. • The segments are numbered 1-8. • The separation of segments is based on its own
dual vascular inflow,biliary drainage and lymphatic drainage. • In general each segment is
wedge shaped with apex directed towards hepatic hilium(porta hepatis) • Segment 1 is
caudate lobe lies posterior around IVC • Segment 1-5 makeup left hemiliver and remaining
 right . • For liver to remain viable, resection occur along hepatic veins and portal vein in the
planes that define boundaries of these segments.
5. 5. INCIDENCE  28/100000 in SEA  10/100000 in SE  5/100000 IN NE  Incidence is increasing
day by day due to -chronic hepatitis B &C virus infection.  -cirrhosis due to any cause.  The
disease is more common in male(4:1)usually in middle age group(50years).
6. 6. AETIOLOGICAL FACTORS COMMON  Viral infection- HEPATITIS B&/C  External source-
alcohol,aflatoxin.  Cirrhosis from any cause.  Non alcoholic steatohepatitis(NASH)  Wide
spread infection with liverflukes- Clonorchis sinensis. UNCOMMON • Primary biliary cirrhosis •
Hemachromatosis • alpha 1Antitrypsin deficiency • Wilson disease
7. 7. Pathogenesis  The exact pathogenesis is unknown.  The disease seems to occur in stages:
Chronic liver injury > cell death >regeneration> cellular metabolic dysfunction> release of
inflammatory mediators> increase risk of transforming mutation of hepatocytes. •
Preneoplastic changes –hepatocytes dysplasia can be seen.
8. 8. Clinical presentation Symptoms: Asymptomatic in early stages,discovered only by screening
(ultrasound and AFP).  Presents with abdominal mass which produces discomfort &dragging
sensation on exercise.  Weakness,malaise,abdominal or chest
pain,vomiting,jaundice,haematemesis.  Anorexia,weightloss –incase of metastasis.
9. 9. Contd…. Sign:  Jaundice  Ascites  Hepatomegaly  Periumbilical collateral veins 
Variceal bleeding  Easy bruising  Hepatic encephalopathy  Shock
10. 10. Contd… Local examination:  Palpable mass in right upper abdomen which is
hard,irregular,tender/nontender.  Hepatic bruit
11. 11. SPREAD Tend to spread by invasion into vasculature mostly portal vein. Highly
metastasis to lymphnode. Lung and bone metastasis in terminal cases.
12. 12. Diagnosis: Diagnosis of HCC is done by : 1. Clinical presentation 2.Investigation 3. Staging
13. 13. 1.Investigation:  Imaging: - Ultrasonography - CT Scan - MRI -Angiography  Liver biposy :
-percutanous aspiration or core biopsy
14. 14. Images of investigation
15. 15. Contd..  Tumor markers: -AFP measurement -viral marker  Liver radio isotope scans 
Liver function test: -serum bilirubin -AST -ALT -ALP -Prothrombin time -Serum albumin
16. 16. Contd..
17. 17. MRI Studies Showing the Effects of Hepatocellular Carcinoma at Different Stages of the
Disease. El-Serag HB. N Engl J Med 2011;365:1118-1127 A: Very early stage (one lesion 1.7cm),
B: early stage (2 lesions 2.4 and 1.2 cm) •C: Intermediate stage (multiple lesions, Childs B), D:
Advanced •(large mass and ascites)
18. 18. 2.Staging: OKUDA staging system Clinical parameters cut off value points Tumor size >50%
<50% 1 0 Ascites Present absent 1 0 Serum albumin(mg/dl) >3 <3 0 1 Serum total
bilirubin(mg/dl) <3 >3 0 1
19. 19. Contd..  STAGE 1 =0  STAGE 2=1-2 points  STAGE 3=3-4 points
20. 20. TNM STAGING
21. 21. Patient assesment: By CHILD-TURCOTTE-PUGH Score Measurements Score 1 2 3
Encephalopathy None Mild Moderate Ascites None Slight Moderate Bilirubin(mg/dl) 1-2 2-3 >3
Albumin(g/dl) >3.5 2.8-3.5 <2.8 Prothrombin time <4 sec 4-6 sec >6 sec
22. 22. Contd..  STAGE A =5-6 points  STAGE B =7-9 points  STAGE C =10-15 points
23. 23. Interpretation: Points Class 1 year survival 10 year survival 5-6 A 100% 85% 7-9 B 81% 57%
10-15 C 45% 35%
24. 24. Screening for HCC  Aim: Early asymptomatic curable.  Methods: AFP (every 6 month) &
Ultrasound  Indications: For patient at risk for HCC:- -Cirrhosis -Hepatitis B,C -Alcohol
consumption -Genetic hemachromatosis -Autoimmune hepatitis -Non alcoholic
steatohepatitis -Primary biliary cirrhosis -Alpha1 antitrypsin deficiency
25. 25. Treatment A. Surgical approach B. Non surgical therapy
26. 26. A. Surgical approach a. Segmental or local resection b. Lobectomy or partial hepatectomy
c. Extended lobectomy d. Liver transplantation
 27. 27. Contd.. First 3 for: Liver transplantation for: Single tumor within single segment Child
Turcotte Stage A Tumor size <5 cm Multiple tumor size of each <3cm Single tumor size<5cm
Multiple tumor sizeof each<3cm No vascular invasion No extrahepatic spread
28. 28. Images of surgical treatment
29. 29. B.Nonsurgical therapy Majority of HCC not be amenable to surgical resection because of :-
=Advanced stage of the carcinoma & =Severity of the underlying liver disease
30. 30. Contd.. The options are: Ablative -Ethanol injection -Acetic acid injection -
Thermal(cryotherapy,readiotherapy,microwave) Transarterial -Embolization -
Chemoembolization Systemic -Chemotherapy -Radiotherapy -Imunotherapy
31. 31. Radiofrequency ablation
32. 32. Transarterial chemo embolization
33. 33. Prognosis after treatment: o5 year survival rate:- 30-40% after liver resection o5year
survival rate:- 75% in liver transplantation o2 year survival rate :- 60% in transarterial
chemoembolization
34. 34. Conclusion In brief ,preventing and treating viral hepatitis may help to reduce the risk of
developing liver cancer.Childhood hepatitis vaccination of hepatitis B may reduce risk of
it.Proper nutrition,rest,good habits(avoid alcohol) and safer practises makes a man healthy.

Functions of the Nervous System

To carry out its normal role, the nervous system has three overlapping
functions.

1. Monitoring changes. Much like a sentry, it uses its millions of

sensory receptors to monitor changes occurring both inside and
outside the body; these changes are called stimuli, and the
gathered information is called sensory input.
2. Interpretation of sensory input. It processes and interprets the
sensory input and decides what should be done at each moment,
a process called integration.
3. Effects responses. It then effects a response by activating
muscles or glands (effectors) via motor output.
4. Mental activity. The brain is the center of mental activity,
including consciousness, thinking, and memory.
5. Homeostasis. This function depends on the ability of the nervous
system to detect, interpret, and respond to changes in the internal
and external conditions. It can help stimulate or inhibit the
activities of other systems to help maintain a constant internal
environment.
 Anatomy of the Nervous System
The nervous system does not work alone to regulate and maintain body
homeostasis; the endocrine system is a second important regulating system.

Organization of the Nervous System

We only have one nervous system, but, because of its complexity, it is difficult
to consider all of its parts at the same time; so, to simplify its study, we divide
it in terms of its structures (structural classification) or in terms of its activities
(functional classification).
Structural Classification

The structural classification, which includes all of the nervous system organs,
has two subdivisions- the central nervous system and the peripheral nervous
system.

 Central nervous system (CNS). The CNS consists of the brain

and spinal cord, which occupy the dorsal body cavity and act as
the integrating and command centers of the nervous system
 Peripheral nervous system (PNS). The PNS, the part of the
nervous system outside the CNS, consists mainly of the nerves
that extend from the brain and spinal cord.
Functional Classification

The functional classification scheme is concerned only with PNS structures.

 Sensory division. The sensory, or afferent division, consists of

nerves (composed of nerve fibers) that convey impulses to the
central nervous system from sensory receptors located in various
parts of the body.
  Somatic sensory fibers. Sensory fibers delivering impulses from
the skin, skeletal muscles, and joints are called somatic sensory
fibers.
 Visceral sensory fibers. Those that transmit impulses from the
visceral organs are called visceral sensory fibers.
 Motor division. The motor, or efferent division carries impulses
from the CNS to effector organs, the muscles and glands; the
motor division has two subdivisions: the somatic nervous
system and the autonomic nervous system.
 Somatic nervous system. The somatic nervous system allows us
to consciously, or voluntarily, control our skeletal muscles.
 Autonomic nervous system. The autonomic nervous system
regulates events that are automatic, or involuntary; this
subdivision, commonly called involuntary nervous system, has two
parts: the sympathetic and parasympathetic, which typically bring
about opposite effects.
Nervous Tissue: Structure and Function

Even though it is complex, nervous tissue is made up of just two principal

types of cells- supporting cells and neurons.

Supporting Cells

Supporting cells in the CNS are “lumped together” as neuroglia, literally mean
“nerve glue”.

 Neuroglia. Neuroglia include many types of cells that generally

support, insulate, and protect the delicate neurons; in addition,
each of the different types of neuroglia, also simply called either
glia or glial cells,has special functions.
 Astrocytes. These are abundant, star-shaped cells that account
for nearly half of the neural tissue; astrocytes form a living barrier
between the capillaries and neurons and play a role in making
exchanges between the two so they could help protect neurons
from harmful substances that might be in the blood.
  Microglia. These are spiderlike phagocytes that dispose of debris,
including dead brain cells and bacteria.
 Ependymal cells. Ependymal cells are glial cells that line the
central cavities of the brain and the spinal cord; the beating of
their cilia helps to circulate the cerebrospinal fluid that fills those
cavities and forms a protective cushion around the CNS.
 Oligodendrocytes. These are glia that wrap their flat extensions
tightly around the nerve fibers, producing fatty insulating
coverings called myelin sheaths.
 Schwann cells. Schwann cells form the myelin sheaths around
nerve fibers that are found in the PNS.
 Satellite cells. Satellite cells act as protective, cushioning cells.
Neurons

Neurons, also called nerve cells, are highly specialized to transmit messages
(nerve impulses) from one part of the body to another.
  Cell body. The cell body is the metabolic center of the neuron; it
has a transparent nucleus with a conspicuous nucleolus; the
rough ER, called Nissl substance, and neurofibrils are
particularly abundant in the cell body.
 Processes. The armlike processes, or fibers, vary in length from
microscopic to 3 to 4 feet; dendrons convey incoming messages
toward the cell body, while axons generate nerve impulses and
typically conduct them away from the cell body.
 Axon hillock. Neurons may have hundreds of the branching
dendrites, depending on the neuron type, but each neuron has
only one axon, which arises from a conelike region of the cell
body called the axon hillock.
 Axon terminals.These terminals contain hundreds of tiny
vesicles, or membranous sacs that contain neurotransmitters.
 Synaptic cleft. Each axon terminal is separated from the next
neuron by a tiny gap called synaptic cleft.
 Myelin sheaths. Most long nerve fibers are covered with a
whitish, fatty material called myelin, which has a waxy
appearance; myelin protects and insulates the fibers and increases
the transmission rate of nerve impulses.
 Nodes of Ranvier. Because the myelin sheath is formed by many
individual Schwann cells, it has gaps, or indentations, called nodes
of Ranvier.
Classification

Neurons may be classified either according to how they function or according

to their structure.
 Functional classification. Functional classification groups
neurons according to the direction the nerve impulse is traveling
relative to the CNS; on this basis, there are sensory, motor,
and association neurons.
 Sensory neurons. Neurons carrying impulses from sensory
receptors to the CNS are sensory, or afferent, neurons; sensory
neurons keep us informed about what is happening both inside
and outside the body.
 Motor neurons. Neurons carrying impulses from the CNS to the
viscera and/or muscles and glands are motor, or efferent,
neurons.
 Interneurons. The third category of neurons is known as the
interneurons, or association neurons; they connect the motor
and sensory neurons in neural pathways.
 Structural classification. Structural classification is based on the
number of processes extending from the cell body.
  Multipolar neuron. If there are several processes, the neuron is a
multipolar neuron; because all motor and association neurons are
multipolar, this is the most common structural type.
 Bipolar neurons. Neurons with two processes- an axon and a
dendrite- are called bipolar neurons; these are rare in adults,
found only in some special sense organs, where they act in
sensory processing as receptor cells.
 Unipolar neurons. Unipolar neurons have a single process
emerging from the cell’s body, however, it is very short and
divides almost immediately into proximal (central) and distal
(peripheral) processes.
Central Nervous System

During embryonic development, the CNS first appears as a simple tube, the
neural tube, which extends down the dorsal median plan of the developing
embryo’s body.

Brain

Because the brain is the largest and most complex mass of nervous tissue in
the body, it is commonly discussed in terms of its four major regions –
cerebral hemispheres, diencephalon, brain stem, and cerebellum.
Cerebral Hemispheres

The paired cerebral hemispheres, collectively called cerebrum, are the most
superior part of the brain, and together are a good deal larger than the other
three brain regions combined.

 Gyri. The entire surface of the cerebral hemispheres exhibits

elevated ridges of tissue called gyri, separated by shallow grooves
called sulci.
 Fissures. Less numerous are the deeper grooves of tissue called
fissures, which separate large regions of the brain; the cerebral
hemispheres are separated by a single deep fissure,
the longitudinal fissure.
 Lobes. Other fissures or sulci divide each hemisphere into a
number of lobes, named for the cranial bones that lie over them.
 Regions of cerebral hemisphere. Each cerebral hemisphere has
three basic regions: a superficial cortex of gray matter, an
internal white matter, and the basal nuclei.
 Cerebral cortex. Speech, memory, logical and emotional
response, as well as consciousness, interpretation of sensation,
and voluntary movement are all functions of neurons of the
cerebral cortex.
 Parietal lobe. The primary somatic sensory area is located in
the parietal lobe posterior to the central sulcus; impulses traveling
from the body’s sensory receptors are localized and interpreted in
this area.
 Occipital lobe. The visual area is located in the posterior part of
the occipital lobe.
 Temporal lobe. The auditory area is in the temporal lobe
bordering the lateral sulcus, and the olfactory area is found deep
inside the temporal lobe.
 Frontal lobe. The primary motor area, which allows us to
consciously move our skeletal muscles, is anterior to the central
sulcus in the front lobe.
 Pyramidal tract. The axons of these motor neurons form the
major voluntary motor tract- the corticospinal or pyramidal tract,
which descends to the cord.
 Broca’s area. A specialized cortical area that is very involved in
our ability to speak, Broca’s area, is found at the base of the
precentral gyrus (the gyrus anterior to the central sulcus).
 Speech area. The speech area is located at the junction of the
temporal, parietal, and occipital lobes; the speech area allows one
to sound out words.
 Cerebral white matter. The deeper cerebral white matter is
compose of fiber tracts carrying impulses to, from, and within the
cortex.
 Corpus callosum. One very large fiber tract, the corpus callosum,
connect the cerbral hemispheres; such fiber tracts are
called commisures.
 Fiber tracts. Association fiber tracts connect areas within a
hemisphere, and projection fiber tracts connect the cerebrum
with lower CNS centers.
 Basal nuclei. There are several islands of gray matter, called the
basal nuclei, or basal ganglia, buried deep within the white
matter of the cerebral hemispheres; it helps regulate the voluntary
 motor activities by modifying instructions sent to the skeletal
muscles by the primary motor cortex.
Diencephalon

The diencephalon, or interbrain, sits atop the brain stem and is enclosed by
the cerebral hemispheres.

 Thalamus. The thalamus, which encloses the shallow third

ventricle of the brain, is a relay station for sensory impulses
passing upward to the sensory cortex.
 Hypothalamus. The hypothalamus makes up the floor of the
diencephalon; it is an important autonomic nervous system center
because it plays a role in the regulation of body temperature,
water balance, and metabolism; it is also the center for many
drives and emotions, and as such, it is an important part of the
so-called limbic system or “emotional-visceral brain”; the
hypothalamus also regulates the pituitary gland and produces
two hormones of its own.
 Mammillary bodies. The mammillary bodies, reflex centers
involved in olfaction (the sense of smell), bulge from the floor of
the hypothalamus posterior to the pituitary gland.
 Epithalamus. The epithalamus forms the roof of the third
ventricle; important parts of the epithalamus are the pineal
body (part of the endocrine system) and the choroid plexus of
the third ventricle, which forms the cerebrospinal fluid.
Brain Stem

The brain stem is about the size of a thumb in diameter and approximately 3
inches long.

 Structures. Its structures are the midbrain, pons, and

the medulla oblongata.
 Midbrain. The midbrain extends from the mammillary bodies to
the pons inferiorly; it is composed of two bulging fiber tracts,
the cerebral peduncles, which convey descending and ascending
impulses.
 Corpora quadrigemina. Dorsally located are four rounded
protrusions called the corpora quadrigemina because they remind
some anatomist of two pairs of twins; these bulging nuclei are
reflex centers involved in vision and hearing.
 
 Pons. The pons is a rounded structure that protrudes just below
the midbrain, and this area of the brain stem is mostly fiber tracts;
however, it does have important nuclei involved in the control of
breathing.
 Medulla oblongata. The medulla oblongata is the most inferior
part of the brain stem; it contains nuclei that regulate vital visceral
activities; it contains centers that control heart rate, blood
pressure, breathing, swallowing, and vomiting among others.
 Reticular formation. Extending the entire length of the brain
stem is a diffuse mass of gray matter, the reticular formation; the
neurons of the reticular formation are involved in motor control
of the visceral organs; a special group of reticular formation
neurons, the reticular activating system (RAS), plays a role in
consciousness and the awake/sleep cycles.
Cerebellum

The large, cauliflower-like cerebellum projects dorsally from under the

occipital lobe of the cerebrum.

 Structure. Like the cerebrum. the cerebellum has two

hemispheres and a convoluted surface; it also has an outer cortex
made up of gray matter and an inner region of white matter.
 Function. The cerebellum provides precise timing for
skeletal muscle activity and controls our balance and equilibrium.
 Coverage. Fibers reach the cerebellum from the equilibrium
apparatus of the inner ear, the eye, the proprioceptors of the
skeletal muscles and tendons, and many other areas.
Protection of the Central Nervous System 

Nervous tissue is very soft and delicate, and the irreplaceable neurons are
injured by even the slightest pressure, so nature has tried to protect the brain
and the spinal cord by enclosing them within bone (the skull and vertebral
column), membranes (the meninges), and a watery cushion (cerebrospinal
fluid).
Meninges

The three connective tissue membranes covering and protecting the CNS
structures are the meninges.

 Dura mater. The outermost layer, the leathery dura mater, is a

double layered membrane where it surrounds the brain; one of its
layer is attached to the inner surface of the skull, forming
the periosteum (periosteal layer); the other, called
the meningeal layer, forms the outermost covering of the brain
and continues as the dura mater of the spinal cord.
 Falx cerebri. In several places, the inner dural membrane extends
inward to form a fold that attaches the brain to the cranial cavity,
and one of these folds is the falx cerebri.
 Tentorium cerebelli. The tentorium cereberi separates the
cerebellum from the cerebrum.
  Arachnoid mater. The middle layer is the weblike arachnoid
mater; its threadlike extensions span the subarachnoid space to
attach it to the innermost membrane.
 Pia mater. The delicate pia mater, the innermost meningeal layer,
clings tightly to the surface of the brain and spinal cord, following
every fold.
Cerebrospinal Fluid

Cerebrospinal fluid (CSF) is a watery “broth” similar in its makeup to blood

plasma, from which it forms.

 Contents. The CSF contains less protein and more vitamin C,

and glucose.
 Choroid plexus. CSF is continually formed from blood by the
choroid plexuses; choroid plexuses are clusters of capillaries
hanging from the “roof” in each of the brain’s ventricles.
 Function. The CSF in and around the brain and cord forms a
watery cushion that protects the fragile nervous tissue from blows
and other trauma.
 Normal volume. CSF forms and drains at a constant rate so that
its normal pressure and volume (150 ml-about half a cup) are
maintained.
 Lumbar tap. The CSF sample for testing is obtained by a
procedure called lumbar or spinal tap;because the withdrawal of
fluid for testing decreases CSF fluid pressure, the patient must
remain in a horizontal position (lying down) for 6 to 12 hours after
the procedure to prevent an agonizingly painful “spinal
headache”.
The Blood-Brain Barrier

No other body organ is so absolutely dependent on a constant internal

environment as is the brain, and so the blood-brain barrier is there to protect
it.

 Function. The neurons are kept separated from bloodborne

substances by the so-called blood-brain barrier, composed of the
least permeable capillaries in the whole body.
 Substances allowed. Of water-soluble substances, only water,
glucose, and essential amino acids pass easily through the walls
of these capillaries.
  Prohibited substances. Metabolic wastes, such as toxins, urea,
proteins, and most drugs are prevented from entering the brain
tissue.
 Fat-soluble substances. The blood-brain barrier is virtually
useless against fats, respiratory gases, and other fat-soluble
molecules that diffuse easily through all plasma membranes.
Spinal Cord

The cylindrical spinal cord is a glistening white continuation of the brain stem.
 Length. The spinal cord is approximately 17 inches (42 cm) long.
 Major function. The spinal cord provides a two-way conduction
pathway to and from the brain, and it is a major reflex center
(spinal reflexes are completed at this level).
 Location. Enclosed within the vertebral column, the spinal cord
extends from the foramen magnum of the skull to the first or
second lumbar vertebra, where it ends just below the ribs.
 Meninges. Like the brain, the spinal cord is cushioned and
protected by the meninges; meningeal coverings do not end at
 the second lumbar vertebra but instead extend well beyond the
end of the spinal cord in the vertebral canal.
 Spinal nerves. In humans, 31 pairs of spinal nerves arise from the
cord and exit from the vertebral column to serve the body area
close by.
 Cauda equina. The collection of spinal nerves at the inferior end
of the vertebral canal is called cauda equina because it looks so
much like a horse’s tail.
Gray Matter of the Spinal Cord and Spinal Roots

The gray matter of the spinal cord looks like a butterfly or a letter H in cross
section.

 Projections. The two posterior projections are the dorsal,

or posterior, horns; the two anterior projections are the ventral,
or anterior, horns.
 Central canal. The gray matter surrounds the central canal of the
cord, which contains CSF.
 Dorsal root ganglion. The cell bodies of sensory neurons, whose
fibers enter the cord by the dorsal root, are found in an enlarged
area called dorsal root ganglion; if the dorsal root or its ganglion
is damaged, sensation from the body area served will be lost.
 Dorsal horns. The dorsal horns contain interneurons.
 Ventral horns. The ventral horns of gray matter contain cell
bodies of motor neurons of the somatic nervous system, which
send their axons out the ventral root of the cord.
 Spinal nerves. The dorsal and ventral roots fuse to form the
spinal nerves.
White Matter of the Spinal Cord

White matter of the spinal cord is composed of myelinated fiber tracts- some
running to higher centers, some traveling from the brain to the cord, and
some conducting impulses from one side of the spinal cord to the other.

 Regions. Because of the irregular shape of the gray matter, the

white matter on each side of the cord is divided into three
regions- the dorsal, lateral, and ventral columns; each of the
columns contains a number of fiber tracts made up of axon with
the same destination and function.
  Sensory tracts. Tracts conducting sensory impulses to the brain
are sensory, or afferent, tracts.
 Motor tracts. Those carrying impulses from the brain to skeletal
muscles are motor, or efferent, tracts.
Peripheral Nervous System

The peripheral nervous system consists of nerves and scattered groups of

neuronal cell bodies (ganglia) found outside the CNS.

Structure of a Nerve

A nerve is a bundle of neuron fibers found outside the CNS.

 Endoneurium. Each fiber is surrounded by a delicate connective

tissue sheath, an endoneurium.
 Perimeurium. Groups of fibers are bound by a coarser connective
tissue wrapping, the perineurium, to form fiber bundles,
or fascicles.
 Epineurium. Finally, all the fascicles are bound together by a
tough fibrous sheath, the epineurium, to form the cordlike nerve.
 Mixed nerves. Nerves carrying both sensory and motor fibers are
called mixed nerves.
 Sensory nerves. Nerves that carry impulses toward the CNS only
are called sensory, or afferent, nerves.
 Motor nerves. Those that carry only motor fibers are motor, or
efferent, nerves.
Cranial Nerves

The 12 pairs of cranial nerves primarily serve the head and the neck.

 Olfactory. Fibers arise from the olfactory receptors in the nasal

mucosa and synapse with the olfactory bulbs; its function is
purely sensory, and it carries impulses for the sense of smell.
 Optic. Fibers arise from the retina of the eye and form the optic
nerve; its function is purely sensory, and carries impulses for
vision.
 Oculomotor. Fibers run from the midbrain to the eye; it supplies
motor fibers to four of the six muscles (superior, inferior, and
medial rectus, and inferior oblique) that direct the eyeball; to the
eyelid; and to the internal eye muscles controlling lens shape and
pupil size.
 Trochlear. Fibers run from the midbrain to the eye; it supplies
motor fibers for one external eye muscle ( superior oblique).
 Trigeminal. Fibers emerge from the pons and form three
divisions that run to the face; it conducts sensory impulses from
the skin of the face and mucosa of the nose and mouth; also
contains motor fibers that activate the chewing muscles.
 Abducens. Fibers leave the pons and run to the eye; it supplies
motor fibers to the lateral rectus muscle, which rolls the eye
laterally.
 Facial. Fibers leave the pons and run to the face; it activates the
muscles of facial expression and the lacrimal and salivary glands;
carries sensory impulses from the taste buds of the anterior
tongue.
 Vestibulocochlear. fibers run from the equilibrium and hearing
receptors of the inner ear to the brain stem; its function is purely
sensory; vestibular branch transmits impulses for the sense of
balance, and cochlear branch transmits impulses for the sense of
hearing.
 Glossopharyngeal. Fibers emerge from the medulla and run to
the throat; it supplies motor fibers to the pharynx (throat) that
promote swallowing and saliva production; it carries sensory
impulses from the taste buds of the posterior tongue and from
pressure receptors of the carotid artery.
 Vagus. Fibers emerge from the medulla and descend into the
thorax and abdominal cavity; the fibers carry sensory impulses
from and motor impulses to the pharynx, larynx, and the
abdominal and thoracic viscera; most motor fibers are
parasympathetic fibers that promote digestive activity and help
regulate heart activity.
 Accessory. Fiber arise from the medulla and superior spinal cord
and travel to muscles of the neck and back; mostly motor fiber
that activate the sternocleidomastoid and trapezius muscles.
  Hypoglossal. Fibers run from the medulla to the tongue; motor
fibers control tongue movements;; sensory fibers carry impulses
from the tongue.
Spinal Nerves and Nerve Plexuses

The 31 pairs of human spinal nerves are formed by the combination of the
ventral and dorsal roots of the spinal cord.

 Rami. Almost immediately after being formed, each spinal nerve

divides into dorsal and ventral rami, making each spinal nerve
only about 1/2 inch long; the rami contains both sensory and
motor fibers.
 Dorsal rami. The smaller dorsal rami serve the skin and muscles
of the posterior body trunk.
 Ventral rami. The ventral rami of spinal nerves T1 through T12
form the intercostal nerves, which supply the muscles between
the ribs and the skin and muscles of the anterior and lateral trunk.
 Cervical plexus. The cervical plexus originates from the C1-C5,
and phrenic nerve is an important nerve; it serves the diaphragm,
and skin and muscles of the shoulder and neck.
 Brachial plexus. The axillary nerve serve the deltoid muscles
and skin of the shoulder, muscles, and skin of superior thorax; the
radial nerve serves the triceps and extensor muscles of the
forearm, and the skin of the posterior upper limb; the median
nerve serves the flexor muscles and skin of the forearm and some
muscles of the hand; the musculocutaneous nerve serves the
flexor muscles of arm and the skin of the lateral forearm; and
the ulnar nerve serves some flexor muscles of forearm; wrist and
many hand muscles, and the skin of the hand.
 Lumbar plexus. The femoral nerve serves the lower abdomen,
anterior and medial thigh muscles, and the skin of the
anteromedial leg and thigh; the obturator nerve serves the
adductor muscles of the medial thigh and small hip muscles, and
the skin of the medial thigh and hip joint.
  Sacral plexus. The sciatic nerve (largest nerve in the body)
serves the lower trunk and posterior surface of the thigh, and it
splits into the common fibular and tibial nerves; the common
fibular nerve serves the lateral aspect of the leg and foot, while
the tibial nerve serves the posterior aspect of leg and foot;
the superior and inferior gluteal nerves serve the gluteal
muscles of the hip.
Autonomic Nervous System

The autonomic nervous system (ANS) is the motor subdivision of the PNS that
controls body activities automatically.

 Composition. It is composed of a specialized group of neurons

that regulate cardiac muscle, smooth muscles, and glands.
 Function. At every moment, signals flood from the visceral
organs into the CNS, and the automatic nerves make adjustments
as necessary to best support body activities.
 Divisions. The ANS has two arms: the sympathetic division and
the parasympathetic division.
Anatomy of the Parasympathetic Division
The parasympathetic division allows us to “unwind” and conserve energy.

 Preganglionic neurons. The preganglionic neurons of the

parasympathetic division are located in brain nuclei of several
cranial nerves- III, VII, IX, and X (the vagus being the most
important of these) and in the S2 through S4 levels of the spinal
cord.
 Craniosacral division. The parasympathetic division is also called
the craniosacral division; the neurons of the cranial region send
their axons out in cranial nerves to serve the head and neck
organs.
 Pelvic splanchnic nerves. In the sacral region, the preganglionic
axons leave the spinal cord and form the pelvic splanchnic nerves,
also called the pelvic nerves, which travel to the pelvic cavity.
Anatomy of the Sympathetic Division
The sympathetic division mobilizes the body during extreme situations, and is
also called the thoracolumbar division because its preganglionic neurons are
in the gray matter of the spinal cord from T1 through L2.

 Ramus communicans. The preganglionic axons leave the cord in

the ventral root, enter the spinal nerve, and then pass through a
ramus communicans, or small communicating branch, to enter a
sympathetic chain ganglion.
 Sympathetic chain. The sympathetic trunk, or chain, lies along
the vertebral column on each side.
 Splanchnic nerves. After it reaches the ganglion, the axon may
synapse with the second neuron in the sympathetic chain at the
same or a different level, or the axon may through the ganglion
without synapsing and form part of the splanchnic nerves.
 Collateral ganglion. The splanchnic nerves travel to the viscera
to synapse with the ganglionic neuron, found in a collateral
ganglion anterior to the vertebral column.

Physiology of the Nervous System

The physiology of the nervous system involves a complex journey of impulses.

Nerve Impulse

Neurons have two major functional properties: irritability, the ability to

respond to a stimulus and convert it into a nerve impulse, and conductivity,
the ability to transmit the impulse to other neurons, muscles, or glands.

 Electrical conditions of a resting neuron’s membrane. The

plasma membrane of a resting, or inactive, neuron is polarized,
which means that there are fewer positive ions sitting on the inner
face of the neuron’s plasma membrane than there are on its outer
 surface; as long as the inside remains more negative than the
outside, the neuron will stay inactive.
 Action potential initiation and generation. Most neuron in the
body are excited by neurotransmitters released by other neurons;
regardless what the stimulus is, the result is always the same- the
permeability properties of the cell’s plasma membrane change for
a very brief period.
 Depolarization. The inward rush of sodium ions changes the
polarity of the neuron’s membrane at that site, an event called
depolarization.
 Graded potential. Locally, the inside is now more positive, and
the outside is less positive, a situation called graded potential.
 Nerve impulse. If the stimulus is strong enough, the local
depolarization activates the neuron to initiate and transmit a
long-distance signal called action potential, also called a nerve
impulse; the nerve impulse is an all-or-none response; it is either
propagated over the entire axon, or it doesn’t happen at all;it
never goes partway along an axon’s length, nor does it die out
with distance as do graded potential.
 Repolarization. The outflow of positive ions from the cell
restores the electrical conditions at the membrane to the
polarized or resting, state, an event called repolarization; until a
repolarization occurs, a neuron cannot conduct another impulse.
 Saltatory conduction. Fibers that have myelin sheaths conduct
impulses much faster because the nerve impulse literally jumps, or
leaps, from node to node along the length of the fiber; this occurs
because no electrical current can flow across the axon membrane
where there is fatty myelin insulation.
The Nerve Impulse Pathway

How the nerve impulse actually works is detailed below.

 Resting membrane electrical conditions. The external face of

the membrane is slightly positive; its internal face is slightly
negative; the chief extracellular ion is sodium, whereas the chief
 intracellular ion is potassium; the membrane is relatively
permeable to both ions.
 Stimulus initiates local depolarization. A stimulus changes the
permeability of a “patch” of the membrane, and sodium ions
diffuse rapidly into the cell; this changes the polarity of the
membrane (the inside becomes more positive; the outside
becomes more negative) at that site.
 Depolarization and generation of an action potential. If the
stimulus is strong enough, depolarization causes membrane
polarity to be completely reversed and an action potential is
initiated.
 Propagation of the action potential. Depolarization of the first
membrane patch causes permeability changes in the adjacent
membrane, and the events described in (b) are repeated; thus, the
action potential propagates rapidly along the entire length of the
membrane.
 Repolarization. Potassium ions diffuse out of the cell as the
membrane permeability changes again, restoring the negative
charge on the inside of the membrane and the positive charge on
the outside surface; repolarization occurs in the same direction as
depolarization.
Communication of Neurons at Synapses

The events occurring at the synapse are arranged below.

ADVERTISEMENTS

 Arrival. The action potential arrives at the axon terminal.

 Fusion. The vesicle fuses with plasma membrane.
 Release. Neurotransmitter is released into synaptic cleft.
 Binding. Neurotransmitter binds to receptor on receiving
neuron’s end.
 Opening. The ion channel opens.
 Closing. Once the neurotransmitter is broken down and released,
the ion channel close.
Autonomic Functioning

Body organs served by the autonomic nervous system receive fibers from both
divisions.

 Antagonistic effect. When both divisions serve the same organ,

they cause antagonistic effects, mainly because their post
ganglionic axons release different transmitters.
 Cholinergic fibers. The parasympathetic fibers called cholinergic
fibers, release acetylcholine.
 Adrenergic fibers. The sympathetic postganglionic fibers, called
adrenergic fibers, release norepinephrine.
 Preganglionic axons. The preganglionic axons of both divisions
release acetylcholine.
Sympathetic Division

The sympathetic division is often referred to as the “fight-or-flight” system.

 Signs of sympathetic nervous system activities. A pounding

heart; rapid, deep breathing; cold, sweaty skin; a prickly scalp, and
dilated pupils are sure signs sympathetic nervous system
activities.
 Effects. Under such conditions, the sympathetic nervous system
increases heart rate, blood pressure, and blood glucose levels;
dilates the bronchioles of the lungs; and brings about many other
effects that help the individual cope with the stressor.
 Duration of the effect. The effects of sympathetic nervous
system activation continue for several minutes until its hormones
are destroyed by the liver.
  Function. Its function is to provide the best conditions for
responding to some threat, whether the best response is to run,
to see better, or to think more clearly.
Parasympathetic Division

The parasympathetic division is most active when the body is at rest and not
threatened in any way.

 Function. This division, sometimes called the “resting-and-

digesting” system, is chiefly concerned with promoting normal
digestion, with elimination of feces and urine, and with conserving
body energy, particularly by decreasing demands on
the cardiovascular system.
 Relaxed state. Blood pressure and heart and respiratory rates
rate being regulated at normal levels, the digestive tract is actively
digesting food, and the skin is warm (indicating that there is no
need to divert blood to skeletal muscles or vital organs.
 Optical state. The eye pupils are constricted to protect the
retinas from excessive damaging light, and the lenses of the eye
are “set” for close vision.

Practice Quiz: Nervous System Anatomy

and Physiology

Here’s a 10-item quiz about the study guide. Please visit our nursing test
bank page for more NCLEX practice questions.

1.The cell body of all sensory neurons is located within the:

A. Dorsal gray horn
B. Dorsal root ganglion
C. Spinal cord
D. Brain

1. Answer: B. Dorsal root ganglion

 B: The cell bodies of the sensory neurons leading to the spinal

cord are located in clusters, the dorsal root ganglia (DRG), next
to the spinal cord.
 A:  Dorsal gray horn is a mass of gray matter found in every
segment of the spinal cord and is responsible for the processing
system of sensory signals that travel within the spinal cord,
 C: The  spinal cord is a long, thin, tubular bundle of nervous
tissue and support cells that extends from the foramen magnum
at the base of the skull to the second lumbar vertebrae.
 D: Brain serves as a command center for the human nervous
system. It receives input from the sensory organs and sends
output to the muscles.
2. Which of the following is referred to as either physical barriers or
physiologic processes (transport system) that separate the circulating
blood from the brain extracellular fluid in the central nervous system
(CNS)?

A. Circle of Willis
B. Blood-brain barrier
C. Corticobulbar projections
D. Lateral corticospinal tract

2. Answer: B. Blood-brain barrier

 B: Blood-brain barrier serves to restrict and control the

movement of substances between the general circulation and
brain extracellular fluid.
 A: The Circle of Willis  is an arterial polygon formed as the
internal carotid and vertebral systems anastomose around the
optic chiasm or chiasma (partial crossing of the optic nerve. It
provides blood to the brain and neighboring structures.
 C: Corticobulbar projections  have several functions including
voluntary control over cranial nerves, relay to the cerebellum,
 activation of other descending pathways and modulation of
sensory processing.
 D:  Lateral corticospinal tract are responsible for controlling the
speed and precision of skilled movements of the hands
3. A male client was involved in a vehicular accident and developed
an amnesia. He is likely having a damaged in which of the following?

A. Hypothalamus
B. Thalamus
C. Cerebrum
D. Hippocampus

3. Answer: D. Hippocampus

 D: The hippocampus is associated mainly with memory,

particularly, long-term memory.
 A: Hypothalamus  controls vital bodily functions such as hunger,
thirst, body temperature, and hormone secretion.
 B: Thalamus influences mood and registers an unlocalized,
uncomfortable perception of pain.
 C: Cerebrum controls brain functions such as language, logic,
reasoning, and creativity.
4. A client went to the emergency department with a possible brain
damage as evidenced by loss of coordination of motor movement, and
staggering, wide based walking. The client is most likely having a damage
in the:

A. Medulla Oblongata
B. Cerebrum
C. Pons

A Complete Neurological Nursing Assessment Guide

 Neurological nursing assessments aid in identifying and diagnosing issues. 
 Neuro exams should be performed routinely in case anything progresses or worsens. 
 A complete understanding of why and how of neurological nursing assessments will not
only help you remember all of the components of the exam, but also make you a better
prepared nurse. 
AMY WHITE
RN, MSN, Chief Nursing Officer
JUNE 10, 2022

A neurological exam, often called a “neuro exam” consists of an assessment or evaluation

of an individual’s nervous system that is often performed by nurses, advanced practitioners,
and physicians.   
The assessment can be completed using instruments, lights, and reflex hammers.   
Some may ask, “is it painful?”  It is a painless assessment that is often completed to
determine if there is any alteration or issues related to the nervous system.   
If the nervous system is damaged, many physical issues may be noted along with a decline
in daily functioning.   
As with any other medical issue, disease, or disorder, the key to preventing long-term
complications is early identification.  Here is a complete guide on the value and correct
method to complete a neurological nursing assessment. 
 Indications For Performing a Neurological
Nursing Assessment
A neurological nursing assessment can be conducted for various reasons anytime there is
the possibility of a disruption of the nervous system due to the following factors: 
 Following a type of trauma 
 Complaints of headaches, fatigue, blurred vision, changes in behavior, changes in
balance, changes in coordination, injury to the head, neck, or back, numbness or tingling
of the arms and/or legs, fever, seizure activity, slurred speech, tremors, weakness, and
decreased movements of the arms and legs 
 Problems with thinking clearly and memory loss 
 
 Completing a Neurological Nursing
Assessment
The nervous system consists of the brain, spinal cord, and the 12 nerves that originate in
the brain.  
It can sometimes be difficult to complete the neurological assessment if one is unsure of
the rationales of each area being assessed.   
Nurses, especially working with those with a possible neurological deficit, must possess
keen observational skills while performing a neurological nursing assessment. It’s important
not overlook an issue that may be causing a problem.   
The following areas are important to focus on when completing a neurological exam: 
Mental Status
Assesses the level of consciousness and interaction with the environment.  Many times, the
nurse or healthcare professional will ask the patient about time, person, and place to
determine if he/she is showing a deficit in one of these areas. 
Sensory
 A sensory exam assesses the patient’s capability of feeling and understanding sensations
and is often performed by using instruments such as a sharp item, dull item, alcohol swabs,
and tuning forks.
Motor Function and Balance
These can be determined by having the patient to “push” and “pull” using their arms and
legs to determine if there is any weakness noted.  Many times after a neurological stroke,
there is weakness noted on one side of the patient versus the other.  Balance can be checked
by having the patient to walk or stand.   
Reflexes
Due to the various types of reflexes noted in newborns and infants, it is important for the
nurses to observe the reflexes for any abnormalities.
Evaluation of Nerves
There are 12 cranial nerves and they each serve a difference capacity and function.
Coordination Exam
This often exhibits itself when the patient begins walking abnormally or cannot do simple
commands such as tapping one’s norse with eyes closed.
 Five Minute Neurological Nursing
Assessment
As nurses and other healthcare providers, it is imperative to attend to neurological needs
quickly.  The following are important when completing the 5-minute neurological nursing
assessment: 
 Mental status – nurses can tell a great deal by looking for odd movements and level of
consciousness 
 Cranial nerves – assessing visual fields, pupil constriction and dilation, speech, and facial
strength  
 Functional motor testing – assessing lower limbs/upper limbs for any weakness or
limitations 
 Gait – ability to walk straight and to maintain balance 
 Sensory and Coordination – sensory testing is purely subjective and coordination can be
caused by many things such as lesions on the brain or sensory disorders 
 Reflexes – reflex testing is purely objective and assess for asymmetries
 Impact of Neurological Nursing
Assessment
The five-minute neurological nursing assessment can quickly identify any issues, thus
preventing progression and providing intervention.  
Nurses are often the first ones to notice any abnormalities and can sometimes stop
something in time before it becomes too aggressive.   
One must understand that a neurological nursing assessment should be completed with
accuracy, thoroughness, and complete understanding of the assessment.   
It is important that a neurological nursing assessment be performed every four hours or
sooner in order to ensure continuity of care and that no adverse effects or changes have
occurred.   
The neurological status of a patient can change abruptly and suddenly, so ensuring that
“neuro checks” are being performed and reported helps predict the outcomes for the patient.   
It also gives reassurance to the family that the best care possible is being administered and
that any subtle changes will be noted by the nurse.   
 The Bottom Line
Neurological nursing assessments should not be delayed or skipped. Important and valid
information can be missed or overlooked and of course, deterioration of the patient’s
condition can unfortunately take place.

Assessment of the Cranial Nerves

The nervous system is a very complex system which is vital to the functioning of the human
body. The nervous system is comprised of the central nervous system (CNS) and peripheral
nervous system (PNS). There are 31 pairs of spinal nerves and 12 pairs of cranial nerves. Below
are the procedures for performing an assessment of the cranial nerves.

For more information about performing a nursing health assessment read the article  Tips for A
Better Nursing Health Assessment . This will help you proceed through an assessment including
the nervous system as you move from head-to-toe.
During a complete health assessment of the nervous system, you will perform an assessment of
the cranial nerves, motor function, sensory function, and reflexes. Below is a complete
assessment of the cranial nerves. Read our article 5 Tips for Performing a Nursing Health
Assessment of the Nervous System   for assessment of the motor function, sensory function, and
reflexes.
Cranial Nerves

DESIGNATIO NUMBE
NERVE TYPE FUNCTION
N R

I 1 Olfactory nerve Sensory The nerve of smell

II 2 Optic nerve Sensory The nerve of vision

III 3 Oculomotor Nerve Motor Muscles of eye movement

IV 4 Trochlear Nerve Motor Muscles of eye movement

V 5 Trigeminal Nerve Mixed For the face and muscle for chewing

VI 6 Abducens Nerve Motor Muscles of eye movement

VII 7 Facial Nerve Motor Facial expression

VIII 8 Vestibulocochlear Sensory Hearing and balance

Nerve

IX 9 Glossopharyngeal Mixed Throat and taste (tongue and pharynx)

Nerve

X 10 Vagus Nerve Mixed The nerves of the thorax and abdominal r

viscera etc)

XI 11 Accessory Nerve Mixed, mostly The nerve of the throat and neck muscles
motor

XII 12 Hypoglossal Nerve Mixed, mostly The tongue muscles.

 DESIGNATIO NUMBE
NERVE TYPE FUNCTION
N R

motor

Cranial Nerve I – Olfactory Nerve

The olfactory nerve is the sensory nerve of smell. Before beginning, have some type of aromatic
substance available such as coffee, toothpaste, peppermint or soap to use as part of the
assessment.

1. Begin by testing the patency of each nostril.

2. The patient should be able to identify the odor on each side of the nose.
3. Avoid noxious stimulants such as ammonia and alcohol wipes.
Cranial Nerve II – Optic Nerve
Next, test the optic nerve. The optic nerve is responsible for visual processes. Assessment of the
optic nerve involves the testing of visual acuity, visual fields, and the ocular fundi.

Testing visual acuity involves testing near and distant vision. Visual fields are tested by
confrontation. Confrontation measures peripheral vision. Test of the ocular fundi requires the
use of an ophthalmoscope.
Testing Near Vision

1. You may test a patient’s near vision by asking the patient to read from a magazine or a
newspaper.
2. Observe how far or close the patient holds the object away from the face.
3. Also, note the position of the patient’s head.
Testing Distant Vision

1. Use a Snelling chart. Proceed in the following manner.

2. Have the patient cover one eye with a card or an eye cover.
3. Have the patient read from the left to the right down the chart starting at the top line.
4. Instruct the patient to read to the smallest line of letters they can see.
5. Have the patient cover the other eye and repeat the steps above.
6. Next, ask the patient to read from top to bottom of the chart to the smallest line that
they can see with both eyes uncovered.
7. If the patient wears corrective lenses or contacts for distant vision, test them first with
eyeglasses or their contact lenses. Then, test them without their glasses or contact
lenses.
8. The results of the tests are recorded as a fraction. The numerator indicates the distance
from the chart which is normally 20 ft. The denominator indicates the distance at
which the person with normal vision can read the last line. The lines on the chart are
numbered.
Normal vision is 20/20. This means the patient is 20 feet away from the chart and can read the
line numbered 20.
If the patient’s vision is 20/30 then the patient reads at 20 ft what a person with normal vision
reads at 30 ft.

Observe the patient while they are reading the chart. If a patient is unable to read more than one-
half of the letters on a line record the number of the line above.
Testing visual fields

Confrontation

1. Have the patient sit or stand about 2-3 ft away from you at eye level.
2. Tell the patient you will be testing their peripheral vision.
3. Have the patient cover one eye with a card.
4. Cover your eye on the same side as the patients.
5. Have the patient look into your uncovered eye.
6. Hold a penlight in your hand above your heads and move the object into the field of
vision.
7. Do this from at least four different directions, downward toward the nose and upward
toward the nose, etc.
8. Have the patient say “now” when they first see the object.
9. Repeat this procedure on the other eye.
10. If the patient cannot see the object at the same time as you, there may be some
peripheral vision loss. This test assumes the nurse has normal peripheral vision. And
remember the patient has a possible neurological dysfunction.
Test the ocular fundi.

1. An ophthalmoscope is used to examine the fundus of the eye. This is mostly an

advanced skill performed by physicians and nurse practitioners but it is good to know
what is occurring doing an ophthalmic examination.
2. During this procedure, you will normally locate the optic disc.
3. Describe the color and shape of the optic disc.
Cranial Nerve III – Oculomotor, Cranial Nerve IV – Trochlear, and
Cranial Nerve VI – Abducens.
The oculomotor nerve, trochlear nerve, and abducens nerve (cranial nerves III, IV, and VI) all
work together, therefore, are assessed together.

During this test, you will assess direct and consensual pupillary reaction to light, convergence,
accommodation of the eyes and the six cardinal points of gaze.

Testing Consensual Pupillary Reaction to Light

1. To perform the direct and consensual pupillary reaction test, dim the lights in the
room.
2. Explain to the patient that you will be shining a light directly at each eye.
3. Explain to the patient that they must stare straight ahead during this procedure.
4. Moving in from the patient’s side, shine the light directly into one eye.
5. Observe for constriction of the illuminated eye.
6. This is a direct pupillary reaction to light.
7. Also, observe the simultaneous reaction of the other pupil. or constriction of the pupil
not illuminated.
8. This is consensual constriction.
9. The illuminated eye should be a little faster and greater than the consensual reaction.
10. Also, during this procedure inspect the patient’s pupil.
11. The pupil should be round, equal in size and shape and in the center of the eye.
Testing accommodation and convergence of pupil response.

1. For accommodation and convergence, you will be testing the muscles of the eye.
2. Ask the patient to stare straight ahead at a distant point.
3. Hold a penlight about 4 to 5in from the patient’s nose, then ask the client to shift the
gaze from the distant point to the penlight.
4. The eyes should turn inward. This is convergence.
5. The pupils also should constrict as the eyes focus on the penlight.
6. The pupillary change is accommodation, a change in the size to adjust vision from far
to near.
A normal response to pupillary testing is recorded as  PERRLA, (pupils equal, round, react to
light, and accommodation).
Testing the six cardinal fields of gaze.
There are two methods used for this assessment. The first is the “H” Method. The second is the
“Wagon Wheel” Method. These procedures test eye movement and the muscles of the eye.

During the procedure, you will be assessing the patient’s ability to follow your movement with
their eyes. Assess the patient eyes while performing the procedure. You are looking for the
presence of any abnormalities such as nystagmus in one or both eyes.  Nystagmus is the rapid
back and forth jerky movement of the eyeball with the rapid lateral movement of the eyeball.
The “H” Method

1. For this procedure, you will need a penlight used as an object for the patient to focus
on.
2. Stand about two feet in front of the patient.
3. Explain to the patient that they must keep their head still and follow the penlight as
you move it in several directions in front of their eyes.
4. You will be drawing an “H” in front of the patient.
5. First, start with the penlight midline.
6. Have the patient focus on the penlight.
7. Now, move the penlight to the left, then straight up and then straight down. (This
movement will form the left half of the “H”)
8. Now drop the penlight from that position and reposition it at the midline again.
9. Have the patient refocus on the penlight.
10. Now move the penlight to the right then straight up and then straight down. (This
movement should form the right side of the “H”)
The Wagon Wheel method

1. For this procedure, you will need a penlight used as an object for the patient to focus
on.
2. Stand about two feet in front of the patient.
3. Explain to the patient that they must keep their head still and follow the penlight as
you move it in several directions in front of their eyes.
4. You will be drawing a wagon wheel or a star shape.
5. Have the patient focus on the penlight.
6. Now, start at midline and move the penlight in the direction to form a star or a wagon
wheel.
7. Example. Move penlight from the middle to–>right upper to–>middle to–> right lower
to–> middle to–>left upper to–>middle to–> right lower until you have made at least
six straight lines.
8. Always return the penlight to the center position before changing directions.
Cranial Nerve V – Trigeminal Nerve
The trigeminal nerve is the main nerve of the face. You will be testing the sensory function of the
nerve. You will be looking for a loss of sensation, pain or any fine rapid muscle movements
called fasciculations.
Test the sensory function of the nerve.

1. Ask the patient to close both eyes.

2. Touch the patient face with a wisp of cotton.
3. Have the patient to say “now” every time they feel the cotton.
4. Repeat this on the patient’s chin and forehead to assess all three branches of the nerve.
Next test the corneal reflex.

1. A patient’s contact lenses will need to be removed.

2. Have the patient look straight ahead.
3. Use a wisp of cotton to touch the patient’s cornea from the side.
4. The patient should blink.
Next, test the motor function of the nerve.
You are assessing for any pain, muscle spasms or deviation of the mandible.

1. Let the patient know you will be touching their face.

2. Palpate the patient’s masseter and temporalis muscles and ask the patient to clench
their teeth tightly.
3. Note the strength of the muscle.
4. Next, ask the patient to open and close the mouth several times.
5. You are looking for symmetry of movement of the mandible and any deviation from
the midline.
Cranial Nerve VII – Facial Nerve
The facial nerve is a motor nerve. This nerve supplies the motor fibers used for facial expressions
and, also the salivary and lacrimal glands.

First, you will be assessing the symmetry of facial movement.

1. To test this nerve you will be asking the patient to make several facial expressions.
2. Have the patient perform the following facial expressions.
A. Smile showing their teeth
B. close both eyes
C. puff their cheeks
D. frown
E. and raising their eyebrows.
Second, test the muscle strength of the upper and lower facial muscles.

1. Have the patient close both eyes tightly and keep them closed.
2. Attempt to open the eyes by retracting the upper and lower eyelids simultaneously.
3. Then, ask the patient to puff their cheeks.
4. Apply pressure to the cheeks attempting to force the air out through the lips.
Third, test the sense of taste.

 Gather 3 cotton-tipped applicators.

 Moisten them and dab one in a sample of sugar, the second in salt and the third in
lemon juice.
 Touch the patient’s tongue with an applicator one at a time and ask the patient to
identify the taste.
 Use water to rinse the mouth between tests.
Cranial Nerve VIII – Vestibulocochlear Nerve
The vestibulocochlear nerve is a sensory nerve and is responsible for transmitting information
about balance and hearing from the inner ear to the brain.
Assess the vestibulocochlear nerve using the Rinne test, the Weber test, and the Romberg test.
The Rinne test compares bone conduction with air conduction. It tests for tinnitus and deafness.
The Weber test provides lateralization of the sound. Lateralization is roughly defined as
localized to one side in the presence of another side. Also, it is used to check for hearing and if a
person hears better in one ear than another.
And the Romberg test assesses coordination and equilibrium. A tuning fork and your watch are
used for the Weber and Rinne test.
Performing the Rinne test.

1. While holding the tuning fork by the handle, gently strike the fork on the palm of your
hand. This will start the tuning fork vibrating.
2. Place the base of the tuning fork on the patient’s mastoid process.
3. Next, ask the patient to tell you when they no longer hear the sound.
4. Note the number of seconds.
5. Then, immediately, while the tuning fork is still vibrating, move the fork in front of
the external auditory meatus. It should be 1 to 2 centimeters from the meatus.
6. Ask the patient to tell you again when they no longer hear the sound.
7. Note the number of seconds again.
8. Compare the time note of air conduction and bone conduction.
9. Normally the sound is heard twice as long by air conduction than by bone conduction.
10. So Air conduction should be 2 X longer than bone conduction. (Ex. Air conduction 30
seconds, bone conduction 15 seconds)
Performing the Weber test.

1. While holding the tuning fork by the handle, gently strike the fork on the palm of your
hand. This will start the tuning fork vibrating.
2. Place the base of the vibrating fork against the patient’s skull. Use the midline of the
anterior portion of the frontal bone or the forehead.
3. Ask the client if the sound is heard equally on both sides or better in one ear than the
other.
4. A normal finding is that the patient hears equally in both ears.
5. Chart this as “no lateralization.”
6. If a patient hears the sound in one ear better than the other, the sound is lateralized.
Ask the patient which ear and document.
Performing the Romberg test.

1. For this test stand near the patient and be prepared to support them if they lose their
balance.
2. Ask the patient to stand with feet together and arms at side.
3. First, begin with eyes open, then have them close their eyes.
4. Wait for about 20 seconds.
5. The patient should be able to maintain this position with only a little swaying.
6. Document this as a negative Romberg. This means it is normal.
Cranial Nerve IX – Glossopharyngeal and Cranial Nerve X – Vagus
Nerve
The glossopharyngeal nerve is a mixed nerve. The motor fibers carry motor information from the
throat to the brain. And the sensory fibers carry impulses from the pharynx and tongue (taste
buds).
The vagus nerve is the largest of the cranial nerves. This nerve provides sensation from the
throat, as well as organs of the chest and abdomen, taste from the tongue and back of the throat,
and muscle function of the palate.
Testing the motor activity of these nerves.

1. Explain to the patient that you are going to place a tongue blade in the mouth.
2. Have the patient open their mouth.
3. Use a tongue blade to depress the patient’s tongue.
4. Ask the patient to say “ah.”
5. Observe the movement of the soft palate and uvula.
6. The soft palate should rise. The uvula should remain midline.
Next, test the gag reflex.

This test assesses the sensory aspect of cranial nerve IX and the motor activity of cranial nerve X.

1. Explain to the patient that you are going to place a tongue blade in the mouth and
lightly touch the throat.
2. Touch the posterior wall of the pharynx with a tongue depressor.
3. Observe the pharyngeal movement.
Finally, test the motor activity of the pharynx.
 1. Ask the patient to drink a small amount of water.
2. Note the ease or difficulty of swallowing.
3. Also, note the quality of the voice. Is there any hoarseness while speaking?
Cranial Nerve XI – Accessory Nerve or Spinal Accessory Nerve
The accessory nerve is a mixed nerve but mostly the motor nerve of the sternocleidomastoid and
trapezius muscles. During this assessment, you will check the strength and movement of the
patient’s sternocleidomastoid and trapezius muscle.

First, test the trapezius muscle.

1. Ask the patient to shrug the shoulders.

2. Observe the quality of the shoulder movement, symmetry of action, and lack of
fasciculations.
3. Test the strength of the trapezius muscle by having the patient shrug the shoulders
while you resist with your hand.
Second, test the sternocleidomastoid muscle.

1. Ask the patient to turn their head to the right and then to the left.
2. Ask the patient to try to touch the right ear to the right shoulder without raising the
shoulder.
3. Repeat on the left side.
4. Observe the range of motion.
5. Test the strength of the sternocleidomastoid muscle by asking the patient to turn their
head to the left against your resisting hand.
6. Repeat the preceding step with the client turning to the right side.
Cranial Nerve XII – Hypoglossal Nerve
The hypoglossal nerve supplies the muscles of the tongue. This assessment involves testing the
movement of the tongue.

1. Ask the patient to protrude the tongue.

2. Now, ask the patient to retract the tongue.
3. Ask the patient to protrude the tongue and move it to the right side and then to the left
side.
4. You are noting the ease and equality of movement.
Next, test the strength of the tongue.

1. Ask the patient to push against the inside of the cheek with a tip of their tongue.
2. Provide resistance by pressing one or two fingers against the patient’s outer cheek.
3. Repeat on the other side.
In conclusion, the tips above will help you with a nursing health assessment of the cranial nerves.
Perform a comprehensive or complete neurological assessment when a neurological concern or
dysfunction is suspected.

A basic check or recheck of the neurological system is done during a normal head-to-toe
assessment. Don’t forget to read 5 Tips for Performing a Nursing Health Assessment on the
Nervous System   for the additional portions of the comprehensive assessment.
Steps
Disclaimer: Always review and follow agency policy regarding this specific
skill.

1. Gather supplies: penlight. For a comprehensive neurological exam, additional

supplies may be needed: Snellen chart; tongue depressor; cotton wisp or
applicator; and percussion hammer; objects to touch, such as coins or paper
clips; substances to smell, such as vanilla, mint, or coffee; and substances to
taste such as sugar, salt, or lemon.
2. Perform safety steps:
o Perform hand hygiene.
o Check the room for transmission-based precautions.
o Introduce yourself, your role, the purpose of your visit, and an estimate
of the time it will take.
o Confirm patient ID using two patient identifiers (e.g., name and date of
birth).
o Explain the process to the patient and ask if they have any questions.
o Be organized and systematic.
o Use appropriate listening and questioning skills.
o Listen and attend to patient cues.
o Ensure the patient’s privacy and dignity.
o Assess ABCs.
3. Obtain subjective assessment data related to history of neurological disease
and any current neurological concerns using effective communication.
4. Assess the patient’s behavior, language, mood, hygiene, and choice of dress
while performing the interview. Note any hearing or visual deficits and ensure
glasses and hearing aids are in place, if needed.
5. Assess level of consciousness and orientation; use Glasgow Coma Scale if
appropriate.
6. (Optional) Complete Mini-Mental State Examination (MMSE), if indicated.
7. Assess for PERRLA.
8. Assess motor strength and sensation.
o Hand grasps
o Upper body strength/resistance
o Lower body strength/resistance
o Sensation in extremities
9. Assess coordination and balance.
o Ask the patient to walk, using an assistive device if needed, assessing
gait for smoothness, coordination, and arm swing.
o As appropriate, assess the patient’s ability to tandem walk (heel to toe),
walk on tiptoes, walk on heels.
o Assess cerebellar functioning using tests such as Romberg, pronator
drift, rapid alternating hand movement, fingertip-to-nose, and heel-to-
shin tests.
10. (Optional) Perform a cranial nerve assessment and assess deep tendon
reflexes as indicated.
11. Assist the patient to a comfortable position, ask if they have any questions,
and thank them for their time.
12. Ensure five safety measures when leaving the room:
o CALL LIGHT: Within reach
o BED: Low and locked (in lowest position and brakes on)
o SIDE RAILS: Secured
o TABLE: Within reach
o ROOM: Risk-free for falls (scan room and clear any obstacles)
13. Perform hand hygiene.
14. Document the assessment findings and report any concerns according to
agency policy.